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In previous work with mouse lines selected for resistance (R) and susceptibility (S) to fescue toxicosis, R mice had higher activities of Phase II liver enzymes glutathione S-transferase and uridine diphosphate glucuronosyl-transferase than S mice. Objectives of this study were: 1. to determine whether selection for toxicosis response had also caused divergence between lines in hepatic Phase I enzyme activity (as assessed by sleep time following sodium pentobarbital anesthesia), 2. to determine whether sleep time differences between lines were modulated by fescue toxins or enzyme inducers in the diet, and 3. to determine whether sleep time differences among individual mice were correlated with the impact of a toxin-containing diet on their post-weaning growth. In experiment 1, five dietary treatments were assigned to 24 male mice in each line: rodent food control, E+ (50% endophyte-infected fescue seed, 50% control), E+P (E+ with 1000 ppm phenobarbital), E- (50% endophyte-free fescue seed, 50% control), and E-P (E- with 1000 ppm phenobarbital). After four weeks on these diets, mice were challenged with a sleep time test. All mice were then switched to a pelleted rodent food diet. Each mouse then received a second sleep time test, a random 1/4 of the population after one, two, three, and four weeks on the standard diet. Results demonstrated that, regardless of dietary treatment, R mice had a shorter sleep time than S mice, suggesting higher activity of liver Phase I microsomal enzymes. Mice that were fed phenobarbital had significantly shorter sleep time than those whose diets did not include this microsomal enzyme inducer. Time interval between the first and second sleep time did not significantly impact the second sleep time, confirming line differences in the absence of toxins and inducers and with advancing age. In experiment 2, male and female R and S mice were fed an E- diet for 2 weeks, then an E+ diet for 2 weeks, followed by a pelleted rodent food diet for 2 weeks. Mice were then administered a sleep time test. Their growth rate response to fescue toxicosis was quantified as the proportional reduction in gain during two weeks on the E+ diet, compared to gain on E- during the previous two weeks. Sleep time was significantly influenced by line but not by sex or the line x sex interaction. As in Experiment 1, S mice slept longer than their R counterparts. The residual correlation between reduction in gain associated with the E+ diet and sleep time was only 0.04. Thus, under these experimental conditions an individual animal's Phase 1 enzyme activity did not predict how severely its growth rate would be depressed by a toxin-containing diet. Based upon these and previous studies, divergent selection for toxicosis response in mice was successful partially by causing divergence between lines both in Phase I and Phase II liver detoxification enzyme activities. If a heritable, practical, and economical criterion could be identified to quantify such differences in livestock species, then selection for toxicosis resistance might contribute to the solution of this important problem for American agriculture. / Master of Science

”Bakgrund: Preoperativ bedömning syftar till att identifiera sjukdomar och risker för anestesiförfarandet och att planera anestesin. Syfte: Att beskriva hur ofta den planerade preoperativa anestesibedömningen ändras vid anestesi induktion. Specifika frågeställningar var om det fanns skillnader i antal ändringar mellan kön, ålder, ASA- klassificering och tid på dygnet för operation. Metod: Retrospektiv journalgranskning som redovisas med deskriptiv statistik. Resultat: Av 177 inkluderade journaler uppvisade 130 (73,4%) en avvikelse från den preoperativa planen till anestesi induktionen. Det fanns ingen signifikant skillnad mellan antalet avvikelser för kön, ålder, ASA -klassificering eller tid på dygnet för operation. Slutsats: Den preoperativt planerade anestesimetoden ändrades vid majoriteten av anestesiinduktionerna.”

Dissertation (PhD)--University of Stellenbosch, 2003. / ENGLISH ABSTRACT: Background to the study OLA can give rise to certain problems: 1. A significant decrease in lung volume is reported to occur in the dependent lung during OLA in the LDP. This decrease in lung volume can result in an acute increase in opposition to RV ejection. The potential problem is that the right ventricle is a thin walled structure that can generate considerably less work than the thicker walled LV. It possesses little reserve to deal with an acute rise in afterload as may occur during acute lung injury or after lung resection. Therefore, this increase in afterload during OLA may potentially impair RV-PA coupling. Albeit this potential problem exists, the changes in RV afterload and how the right ventricle performs during OLA have not been well studied. 2. Arterial hypoxemia, due mainly to venous blood being shunted via the non-ventilated lung, may present a clinical problem during one lung ventilation. a. The relative resistances of the pulmonary vascular beds of the dependent ventilated and nondependent non-ventilated lungs are an important factor governing shunting and thus arterial oxygenation during one lung anesthesia. A high non-ventilated lung PVR and low ventilated lung PVR will facilitate good arterial oxygenation during OLA. An increase in non-ventilated lung PVR is governed predominantly by hypoxic pulmonary vasoconstriction. A low opposition to pulmonary blood flow in the dependent lung is facilitated predominantly by a high alveolar oxygen tension and normal lung volume, albeit other factors also play a role in this regard. b. The saturation and oxygen content of mixed venous blood will contribute significantly to the arterial oxygenation in the presence of a large shunt as occurs during OLA. i. On the one hand, venous desaturation as a cause of hypoxemia during one lung anesthesia has not as yet been systematically addressed in the literature. ii. On the other hand, if RV afterload increases to such a degree that it leads poor RV performance, this may cause impairment of global circulatory efficiency and lead to mixed venous desaturation. The question that has been raised is whether inotrope infusions could improve RV and LV performance, cardiac output, and thereby the efficiency of the circulation. Increases in the efficiency of the circulation will result in an improvement in mixed venous and arterial oxygenation in the presence of a large shunt. Nonetheless, the administration of inotrope infusions in the presence of a shunt and during OLA has been reported to aggravate hypoxemia. Thus at the time of conducting the study, conflicting reports of whether increasing cardiac output and thereby mixed venous oxygenation would increase or decrease arterial oxygenation during OLA In the light of the above, the researcher thus investigated RV afterload, RV performance and coupling to its load during OLA. The study also addressed the question whether different levels of inotrope infusion or PEEP hadbeneficial or deleterious effects on RV afterload, RV performance and coupling to its load during OLA. Furthermore, if cardiac output increased during OLA secondary to the infusion of inotropes, would this improve the efficiency of the circulation, mixed venous oxygenation and thus the arterial oxygenation during OLA, or would it worsen shunt and arterial oxygenation during OLA? Control group: OLA and the opposition to pulmonary flow Pulmonary arterial elastance increased by between 18 to 36% during OLA and mean PAP rose by 32% after initiation of OLA This increase in mean PAP on initiation of OLA is greater than that observed by certain investigators but similar to that seen previously in patients with damaged lungs. The question arose as to why pulmonary artery pressure rises during OLA? From consideration of Ohm’s law, pressure may be regarded as the product of flow and resistance (Mark, Slaughter et al. 2000). The increase in mean PAP during OLA is due to two reasons. 1. Firstly, the pressure versus flow curve is likely to be steeper during OLA. This is because pulmonary vascular recruitment and dilatation (pulmonary vascular reserve) is more limited in scope in these patients than is usual and most likely accounts for the increase in pulmonary artery pressure during OLA. The reasons for the limited pulmonary vascular reserve in the DL during OLA include: a. The pulmonary vascular bed of patients subjected to OLA is frequently abnormal because of its underlying pathology, b. During OLA in the lateral decubitus position, lung volume decreases to a greater degree than during two-lung anesthesia (Klingstedt, Hedenstierna et al. 1990). c. This decrease in lung volume will be further aggravated by DLT malpositions, secretions and blood, and absorption atelectasis due to the use of high concentrations of oxygen (Hedenstierna 1998; Krucylak, Naunheim et al. 1996). d. Excessive amounts of extrinsic or intrinsic PEEP during OLA can compress the intra-alveolar capillaries and deleteriously affect the pulmonary vascular resistance (Ducros, Moutafis et al. 1999; Inomata, Nishikawa et al. 1997; Bardoczky, Yernault et al. 1996; Yokota, Toriumi et al. 1996). 2. Secondly, there is greater flow through this vascular bed that possesses a higher resistance. It is noteworthy that the increase in mean PAP did not exceed a value of 25 mm Hg during OLA, even though cardiac output increased by 30%. However, in studies conducted in patients with “damaged lungs”, greater increases in PA pressure (accompanied by a decrease in RVEF) have been reported to occur on PA ligation. A question arises as to why differences exist between PA clamping and OLA? The answer may well be that the observed plateau in the rise of PA pressure during OLA is as a result of progressive diversion of flow to the NDL as PA pressure rises. Support for such a suggestion comes from the observation that concomitant with increases in PA pressure during OLA, HPV is progressively inhibited and shunt fraction progressively rises. This increase in shunt fraction that has been observed to occur as PA pressure rises, reflects an increase in diversion of pulmonary blood flow to the NDL. The impact of diversion of this blood to the NDL is that it possibly acts as a safety mechanism limiting increases in PA pressure and other indices of opposition to pulmonary flow during OLA. This “blow-off effect” will protect the RV until PA clamping occurs.Control group: OLA and RV function The current study represented the opportunity to investigate the significance of the abovementioned increases in PA pressures and elastance on RV performance during OLA. The current study indicates that at the moderate (30%) increases in PAP that accompanied the initiation of OLA, RV performance, as judged by stroke volume, cardiac index, RVEF and RVSWI, did not deteriorate compared to the baseline awake status. In fact, cardiac output increased following surgical incision: this was probably due to sympathetic nervous system stimulation. This observation also fits in with other studies in which RV performance usually only begins to deteriorate when indices of opposition to RV ejection reach 200 to 250% of baseline. Furthermore, a constant preload, as indicated by unchanged central venous and pulmonary artery wedge pressures, and right ventricular end-diastolic volumes were observed throughout the study period. In other words, this increase in RV afyterlad did not cuse the RV to dilate durign OLA. The relationship between stroke work and afterload will vary, depending on the contractile reserve of the ventricle. In this regard, it could be concluded that under the conditions operative in the current study, the RV was operating on the upslope of the RVSWI versus Ea relationship. This supports the observation that RV function is well preserved during OLA. In conclusion, regarding the indices of opposition to pulmonary flow and RV performance during OLA, it can be concluded that: 1. Opposition to RV ejection increases. This is evidenced by a 30% rise in mean PAP and 18 to 36% increase in pulmonary arterial elastance. 2. Right ventricular performance as indicated by RVSWI, RVEF and stroke volume does not decrease during OLA compared with when the patients awake or subjected to two-lung anesthesia. 3. Furthermore, coupling between the RV and its load is well preserved during OLA. This would imply that the RV operates at close to maximal efficiency during OLA and that RV stroke work reserve is present during OLA. It is likely that the RV, which continues operating as a flow pump as it does in normal life, easily copes with the small increases in RV afterload during OLA. Dobutamine during OLA: opposition to pulmonary flow and RV performance The effects of dobutamine infusions on RV performance during OLA can be summarised as follows: 1. Low rates of dobutamine infusion (3 ug.kg-1.min-1) increased cardiac output, stroke volume, and RVSWI. The administration of dobutamine 3 ug.kg-1.min-1 was not accompanied by increases in RV afterload. Therefore, low infusion rates of dobutamine did benefit RV-PA coupling during OLA. 2. However, administration of higher dosages of dobutamine (5 and 7 ug.kg-1.min-1) during OLA was associated with increases in certain indices of opposition to pulmonary blood flow. For example, PA elastance, mean PA pressure, and PVR increased by 30% to 40% compared to both when the patients were awake and when both lungs were being ventilated. Furthermore, PA compliance decreased by up to 61% when dobutamine 5 and 7 ug.kg-1.min-1 were infused compared to the OLA step when dobutaminewas not administered. The increases in mean PAP and PVR are considered to be of limited clinical significance. However, the decrease in PA compliance during the infusion of the highest dosage of dobutamine is clinically significant. PA compliance represents one of the factors determining vascular impedance in the Windkessel model of the circulation. The increases in opposition to pulmonary flow and lack of progressive increase in indices of RV performance are in contrast to what is expected to occur on administration of increasing dosages of the inotrope and pulmonary vasodilator, dobutamine. The reasons for the increase in opposition to pulmonary flow include exhaustion of the pulmonary vascular reserve during OLA at the high cardiac indices of 5 to 5.5 l.min-1.m-2. This aspect overshadowed the expected pulmonary vasodilator effects of dobutamine. Moreover, it is probable that the increase in RV afterload was significant enough to prevent right ventricular performance increasing as would be expected with the administration of progressively higher dosages of inotrope. While dobutamine was being administered during OLA, mean PAP increased to a maximum of 24.9 ± 6.2 mm Hg at a cardiac index of 5.5 ± 1.2 l.min-1.m-2. However during OLA, in the control group, mean PAP was 24.0 ± 7.7 mm Hg at the maximum cardiac index of 4.4 ± 1.1 l.min-1.m-2. This represented a relatively limited rise in PA pressure compared with administration of dobutamine alone. The most likely reason why there may have been a limited increase in mean PAP while dobutamine was being administered is that the “blow off” effect of the NDL vasculature limited the rise in PA pressure. Oxygenation during OLA With regard to oxygen flux, venous and arterial oxygenation during OLA in the control group, the following was observed: 1. Induction of anesthesia and the approximately 1O Celsius decrease in temperature induced an approximately 40% decrease in VO2 that continued during OLA. 2. Initiation of OLA resulted in an increase in cardiac output compared to baseline OLA and awake states. 3. The consequence was an increase in S􀀀��������O2 from 75% and P􀀀��������O2 from 5.4 kPa when the patients were awake to a P􀀀��������O2 of 9.0 ± 1.7 kPa and S􀀀��������O2 of 90.6 ± 4.7% during one-lung anesthesia. 4. During OLA, the significant increase in venous oxygenation resulted in an increase in arterial oxygenation compared to the awake state in spite of the approximately 37% shunt occuring during OLA. 5. Under conditions in the present study, dobutamine administration during OLA did not improve, but maintained the already high venous and arterial oxygenation compared with OLA alone. Therefore, the study hypothesis, that dobutamine would induce improvement in RVF and the increase in cardiac output during OLA would improve arterial oxygenation, does not hold in the current study. The hypothesis that dobutamine administration and improving cardiac output during OLA would increase arterial oxygenation was therefore rejected. However, the rejection of the hypothesis means that the findings of the current study are in contrast to the findings of Mathru et al, and Nomoto and Kawamura. These authors demonstrated that inotrope administration resulted in an increase in arterial oxygenation. Nonetheless, the different results are not at odds with each other. In fact, these differences help to clarify the effect of increases in cardiac output on arterial oxygenation in the presence of asignificant shunt. The differences between the studies can be explained in the following way. Conditions in the current study resulted in a favourable DO2/VO2 ratio and a high starting P􀀀��������O2 even before dobutamine administration was commenced. Therefore the venous saturations were on the flat part of the oxygen dissociation curve and also on the flat part of the relationship between cardiac output and arterial oxygen content originally described by Kelman, Nunn and colleagues. Further increases in cardiac output and the DO2/VO2 ratio would not be expected to, and did not, increase P􀀀��������O2, S􀀀��������O2, or C􀀀��������O2. Thus, arterial oxygenation content and saturation did not change subsequent to the increase in cardiac output associated with the administration of dobutamine in the current study. In contrast, in the Mathru study, the low starting venous saturations and tensions were improved by increases in the DO2/VO2 ratio. As the starting venous saturation was “low,” significant benefit in arterial oxygenation was obtained on increasing cardiac output in that study. One significant concern for the clinician regarding the administration of the inotrope dobutamine during OLA is that it may increase shunt fraction (Qs/Qt) and thereby decrease arterial oxygenation during one lung ventilation. The influence of dobutamine on arterial oxygenation during OLA may theoretically be related to the balance of the following divergent effects: 1. By improving the relationship between oxygen delivery and consumption, dobutamine increases P􀀀��������O2. This increase will benefit arterial oxygenation in the presence of a large shunt, 2. The above has to be weighed against possible increases in VO2 induced by dobutamine, the consequence of which will be a decrease in P􀀀��������O2. Such increases in VO2 were not seen on administration of dobutamine in the current study, 3. An increase in PA pressure accompanying the increased cardiac output will oppose HPV and increase shunt in both the dependent and non-dependent lungs, 4. Direct inhibition of HPV by dobutamine and, 5. The influence of P􀀀��������O2 on HPV (i.e. high levels of venous oxygenation will inhibit whereas low levels will potentiate HPV). Nonetheless, in spite of the concerns (risk) of hypoxemia on administering dobutamine during OLA, dobutamine administration did not decrease PaO2 or arterial oxygen saturation, and neither did it increase the cost of oxygenation compared to when OLA was conducted in the absence of dobutamine infusions. In addition, the findings of studies conducted by Mathru and colleagues, Nomoto and Kawamura and the current study indicate that under usual clinical conditions present during OLA in the LDP, the administration of low dosages of dobutamine do not increase shunt fraction. In fact, the beneficial effect of the increase in cardiac output on venous oxygenation resulted in an increase in arterial oxygenation in the study by Mathru and colleagues; similar mechanisms were most likely operative in the study conducted by Nomoto and Kawamura. Therefore, there is currently no evidence that the administration of dobutamine in dosages of up to 7 ug.kg-1.min-1 increases shunt and worsens arterial oxygenation in humans subjected to OLA in the LDP. It is apparent that the vasodilatory effects of dobutamine resulting in a possible increase in shunt fraction (Qs/Qt) is therefore not the only factor to consider when studying its effects on arterial oxygenation. What is also of great relevance whenconsidering the effects of an inotrope on arterial oxygenation is the effect of inotropic drugs on the venous oxygen content. It is possible that Qs/Qt could be increased by the administration of inotrope. Nonetheless, if venous oxygenation is favourably affected by the administration of dobutamine, then a depressant effect on arterial oxygenation by an increase in the amount of blood passing via the shunt may be negated. If the increase in venous oxygenation is very significant, there may even be benefits in terms of arterial oxygenation, as was the case in the current study. This approach to how the quality of the blood passing via the shunt affects arterial oxygenation shifts the emphasis on prevention and treatment of hypoxemia during OLA from the lung to the efficacy of the circulation. In other words, the emphasis is shifted from what predominantly happens to the non-ventilated lung (HPV) to primarily the efficacy of oxygen flux during OLA. Extrinsic and intrinsic PEEP and OLA The effects of PEEP on hemodynamics and oxygenation observed during OLA in the current study may be summarised as follows. When PEEP5 was applied to the DL during OLA in the current study: 1. Neither right ventricular function, hemodynamics, oxygen flux nor arterial oxygenation was affected by the application of PEEP5 compared to the step when no external PEEP was applied. 2. Significant amounts of intrinsic PEEP were present during OLA in the control group patients. The degree of intrinsic PEEP was weakly related to the degree of obstructive airways disease present on preoperative LFT’s. 3. The most likely reason why PEEP5 did not make a difference to oxygenation or hemodynamics was the existence of similar amounts of intrinsic PEEP during OLA. These findings confirm Myles’s contention that low levels of intrinsic PEEP may have salutary effects on oxygenation during OLA. When PEEP10 was applied to the DL during OLA in the current study, it led to a decrease in stroke volume. This decrease is predominantly due to a decrease in preload, as PVR does not increase to levels that are known to impair RV performance. The decrease in the DO2/VO2 ratio that was induced by PEEP10 predictably decreases P􀀀��������O2 and can potentially lead to impairment of arterial oxygenation. It can therefore be concluded that greater (excessive) amounts of PEEP under more unfavourable circulatory conditions than were observed in the current study, may have deleterious cardio-respiratory effects. In summary, optimising DL volume plays an important role in determining arterial oxygenation. However, the therapeutic index for PEEP is narrow and the anesthesiologist needs to know firstly when the lung volume of the DL approaches FRC and secondly, how to avoid dynamic hyperinflation of that lung. One significant problem is that the best method of monitoring FRC during OLA is not clear at present. / AFRIKAANSE OPSOMMING: Agtergrond tot die studie Eenlongnarkose mag tot sekere probleme aanleiding gee. ’n Betekenisvolle afname in volume van die onderlong vind in die laterale decubitus posisie tydens eenlongnarkose plaas. Hierdie afname in longvolume mag egter ’n akute verhoging in regter ventrikulêre nalading tot stand bring. Die probleem is egter dat die regter ventrikel ’n dunwandige struktuur is wat potensieel baie minder werk as die dikwandige linker ventrikel kan genereer. Die regter ventrikel het min reserwe om ’n akute verhoging in nalading te weerstaan soos wat gebeur met akute longbesering of na longreseksie. Dus die verhoging in nalading wat gepaard gaan met eenlongnarkose mag die koppeling tussen die regter ventrikel en die pulmonale arterie belemmer. Alhoewel hierdie potensiële probleem bestaan, is die verandering albei in regter ventrikulêre nalading en hoe die regter ventrikel funksioneer tydens eenlongnarkose nog nie goed bestudeer nie. 1. Arteriële hipoksemie, hoofsaaklik te wyte aan die groot aftakking via die long wat nie geventileer word nie, mag kliniese probleme tydens eenlongnarkose teweegbring. 2. Die weerstand wat die pulmonale vaskulêre beddens van die geventileerde en nie-geventileerde longe bied teen bloedvloei is belangrike faktore wat aftakking en dus arteriële oksigenasie tydens eenlongnarkose beheer. ’n Hoë weerstand van die nie-geventileerde long en ’n lae weerstand van die geventileerde long se pulmonale vaskulêre beddens sal bevredigende arteriële oksigenasie tydens eenlongnarkose fasiliteer. ’n Verhoging in die pulmonale vaskulêre weerstand van die nie-geventileerde long is hoofsaaklik te wyte aan hipoksiese pulmonale vasokonstriksie. ’n Lae pulmonale vaskulêre weerstand in die geventileerde onderlong is hoofsaaklik gefasiliteer deur ’n hoë alveolêre suurstofspanning en ’n normale long volume, alhoewel alle faktore ook ’n rol in hierdie verband speel. 3. In die teenwoordigheid van die groot aftakking wat bestaan tydens eenlongnarkose, sal die saturasie en suurstof inhoud van gemeng veneuse bloed ’n betekenisvolle bydrae aan arteriële oksigenasie maak. a. Veneuse saturasie as ’n oorsaak van hipoksemie tydens eenlongnarkose, is nog nie sistematies in die literatuur ondersoek nie. b. Indien regter ventrikulêre nalading tot so ’n mate verhoog dat dit tot swak ventrikulêre uitwerp lei, mag dit ’n oorsaak wees van ontoereikendheid van die globale bloedsomloop en tot gemeng veneuse desaturasie lei. Die vraag is dus of verhoging van die kardiale omset deur inotrope ondersteuning die toereikendheid van die sirkulasie kan verbeter. Verbeterde sirkulasie toereikendheid sal tot ’n verhoging in gemeng veneuse en arteriële oksigenasie lei in die teenwoordigheid van ’n groot aftakking. Nietemin, die toediening van inotrope in die teenwoordigheid van ’n groot aftakking tydens eenlongnarkose gerapporteer om hipoksemie te vererger tydens eenlongnarkose. Dus ten tye van die uitvoer van dié studie, is daar uitdrukking gegee tot teenstrydige opinies in die literatuur oftewel verhoging in kardiale omset arteriële oksigenasie sal verbeter of versleg tydens eenlongnarkose.In die lig van die agtergrond hierbo, het die navorser dus regter ventrikulêre nalading, regter ventrikulêre funksie en koppeling van die regter ventrikel met sy lading tydens eenlongnarkose ondersoek. Die studie het ook die vraag benader of inotroop infusies of PEEP goeie of slegte gevolge sou hê op regter ventrikulêre nalading, regter ventrikulêre funksie en koppeling van die regter ventrikel aan sy lading tydens eenlongnarkose. Sou die kardiale omset en die toereikendheid van die sirkulasie sou verbeter sekondêr tot die toediening van inotrope tydens eenlongnarkose, gemeng veneuse oksigenasie en dus arteriële oksigenasie tydens eenlongnarkose verbeter, of sou dit aftakking en arteriële oksigenasie versleg tydens eenlongnarkose? Kontrole groep Pulmonêre elastansie het tussen 18 en 36% verhoog en gemene pulmonale arterie druk het met 32% tydens eenlongnarkose vermeerder. Die verhoging in gemene pulmonale arterie druk met die aanvang van eenlongnarkose is groter as die waardes gesien deur sekere navorsers maar gelyk met waardes gevind in pasiënte met beskadigde longe. Die vraag ontstaan dan hoekom styg pulmonale arterie druk tydens eenlongnarkose? volgens Ohm se Wet, mag druk as die veelvoud van vloei en weerstand beskou word. Die verhoging in gemene pulmonale arterie druk tydens eenlongnarkose is daarvolgens hoofsaaklik te wyte aan twee redes. 1. Eerstens, die kurwe van druk teenoor vloei is waarskynlik styler tydens eenlongnarkose. Hierdie is omdat pulmonale vaskulêre werwing en verwyding (pulmonale vaskulêre reserwe) is meer beperk as nornaal in pasiënte met longsiekte. Hierdie is die waarskynlikste rede hoekom pulmonale arterie druk tydens eenlongnarkose verhoog. Die redes hoekom die pulmonale vaskulêre reserwe in die onderste long tydens eenlongnarkose beperk is sluit in die volgende: 1.1 Die pulmonale vaskulêre bed van pasiënte onderwerp aan eenlongnarkose mag abnormaal wees weens die onderliggende long patologie, 1.2 Tydens eenlongnarkose in die laterale decubitus posisie, is long volume in hoë mate verminder as tydens tweelongnarkose, 1.3 Die voorafgenoemde vermindering in longvolume sal verder verminder word deur wanposisies van die dubbellumenbuis, sekresies en bloed, en absorpsie atelektase. 1.4 Te hoë vlakke van PEEP, oftewel intrinsiek of ekstrensiek van oorsprong, sal die intraalveolêre vate toedruk en so die pulmonale vaskulêre weerstand verhoog. 2. Tweedens, is daar groter vloei deur hierdie vaskulêre bed wat ‘n hoër weerstand bevat. Dit is opmerkingswaardig dat die verhoging in gemene pulmonale arterie druk ‘n waarde van 25 mmHg nie oorskry het nie tydens eenlongnarkose, alhoewel kardiale omset met 30% verhoog het. In pasiënte met beskadigde longe, het vorige studies egter bewys dat groter verhoging in PA druk gebeur tydens afbinding van die pulmonale arterie. Die vraag ontstaan dus hoekom daar verskille bestaan tussen wat gebeur tydens afbind van die pulmonale arterie en eenlongnarkose? Die antwoord mag wees dat die beperking in die styging in PA druk tydens eenlongnarkose as gevolg van ‘n progressiewe afleiding van bloedvloei na die nie-geventileerde long gebeur sodra pulmonale arterie druk styg tydens eenlongnarkose. Die implikasie van die afleiding van bloed na die nie geventileerde long is dat dit as ‘n veiligheids meganisme optree en verdere styging in pulmonale arterie druk beperk tydens eenlongnarkose. Hierdie afblaas meganisme sal die regter ventrikel beskerm tot en met PA afbind.Kontrole groep: eenlongnarkose en regter ventrikulêre funksie Die huidige studie bied die geleentheid om die betekenis van die voorafgenoemde verhoging in PA drukke en elastansie op regter ventrikulêre funksie tydens eenlongnarkose te ondersoek. Die huidige studie dui aan dat die 30% verhoging in pulmonale arterie druk wat met die aanvang van eenlongnarkose plaasvind, glad nie regter ventrikulêre funksie belemmer nie indien dit vergelyk word met die basislyn wakker staat. In teendeel, kardiale omset het verhoog na chirurgiese insnyding: hierdie verhoging is waarskynlik te wyte aan simpatiese senuwee stimulasie na die chirurgiese insnyding. Hierdie waarnemings pas in ook met ander studies waartydens regter ventrikulêre ejeksie alleenlik begin om af te neem indien die indekse van opposisie tot regter ventrikulêre ejeksie 200 tot 250% van basislyn bereik. Verder, die induksie van voorlading, naamlik sentrale veneuse druk, pulmonale arterie wigdruk en regter ventrikulêre einddiastoliese volumes is onveranderd tydens die huidige studie; dit beteken die ventrikel het nie gedilateer het nie tydens die verhoging in regter ventrikulêre nalading. Die verband tussen slagwerk en nalading sal varieer, afhanklik van die kontraktiele status van die ventrikel. In hierdie opsig, kon ons aflei dat die regter ventrikel, onder omstandighede wat tydens diė studie plaasgevind het, gefunksioneer het op die stygende been van die verband tussen regter ventrikulêre slagwerk en pulmonale arterie elastansie. Hierdie waarneming ondersteun die argument in die vorige paragraaf dat die regter ventrikel funksie behoue is tydens eenlongnarkose. Ter opsomming omtrent die indekse van opposisie tot pulmonale vloei en regter ventrikulêre funksie tydens eenlongnarkose: 1. Opposisie tot regter ventrikulêre uitwerp verhoog. Die bewys hiervoor is ’n 30% verhoging in gemene pulmonale arterie druk en ’n 36% verhoging in pulmonale arterie elastansie. 2. Ten spyte van die verhoging in weerstand teen RV uitwerping, het regter ventrikulêre funksie (soos bepaal deur regter ventrikulêre slagwerk indeks, regter ventrikulêre ejeksie fraksie en slag volume), nie verminder tydens eenlongnarkose in vergelyking met die waardes verkry wanneer die pasiënte wakker is of aan tweelongnarkose onderwerp is. 3. Ons kon ook aflei dat die koppeling tussen die regter ventrikel en sy lading goed behoue is tydens eenlongnarkose. Die implikasie hiervan is dat regter ventrikulêre slagwerk reserwe teenwoordig is tydens eenlongnarkose. Tydens eenlongnarkose funksioneer die regter ventrikel as ’n vloeipomp, net soos in normale lewe; dit beteken dat en die klein verhoging in regter ventrikulêre nalading wat ondervind word tydens eenlongnarkose maklik getolereer word. Dobutamien tydens eenlongnarkose: opposisie tot pulmonale vloei en regter ventrikulêre funksie Die uitwerking van dobutamien op regter ventrikulêre funksie tydens eenlongnarkose kan as volg opgesom word: 1. Lae dosisse dobutamien (3 μg.kg-1.min-1) verhoog kardiale omset, slagvolume en regter ventrikulêre slagwerkindeks. Die toediening van dobutamien 3 μg.kg-1.min-1 het nie saamgegaan met ‘n verhoging in regter ventrikulêre nalading nie. Dus, lae dosisse van dobutamien het wel die koppeling tussen die regter ventrikel en die pulmonale vaskulatuur tydens eenlongnarkose verbeter.2. Nietemin, albei die hoër dosisse van dobutamien (5 en 7 μg.kg-1.min-1) tydens eenlongnarkose het verhogings in die opposisie tot pulmonale bloedvloei teweeggebring. Byvoorbeeld, PA elastansie, gemene PA druk en pulmonale vaskulêre weerstand het met 30 tot 40% verhoog in vergelyking met die waardes gekry toe die pasiënte wakker was en toe albei longe geventileer is. ’n Belangrike opmerking in hierdie opsig is dat pulmonale arterie vervormbaarheid tydens eenlongnarkose met 61% verminder het tydens albei dobutamien 5 en 7 μg.kg-1.min-1. Die verhogings in gemene pulmonale arterie druk en pulmonale vaskulêre weerstand is, volgens mening, nie van kliniese of statistiese betekenis nie, alhoewel die vermindering in PA vervormbaarheid tydens die dobutamien 7 μg.kg-1.min-1 infusie wel van kliniese betekenis is. PA vervormbaarheid weerspieël een van die faktore wat vaskulêre impedansie in die 3- element Windkessel model van sirkulasie het. Die verhoging in opposisie tot pulmonale vloei en die afwesigheid van progressiewe verhogings in indekse van regter ventrikulêre funksie is nie wat verwag word indien die dosisse van die inotroop en pulmonale vasodilator dobutamien, progressief verhoog word. Die redes hoekom die opposisie tot pulmonale vloei verhoog tydens die toediening van dobutamien sluit in die uitwissing van die pulmonale vaskulêre reserwe tydens eenlongnarkose. Tydens die hoë kardiale indekse van 5 tot 5.5 μg.kg-1.min-1. is die pulmonale vaskulêre reserwe uitgeput en die meganisme het die verwagte pulmonale vaskulêre vasodilatasie van dobutamien oorskadu. Bowendien is dit waarskynlik dat die verhoging in regter ventrikulêre nalading betekenisvol genoeg was om te verhoed dat regter ventrikulêre funksie progressief verhoog soos sou verwag word met die administrasie van hoër dosisse inotroop. Die administrasie van dobutamien tydens eenlongnarkose het gemene pulmonale arterie druk verhoog tot ’n maksimum van 24,9 ± 6.2 mm Hg teen ’n kardiale indeks van 5.5 ± 1.2 l.min-1.m2. Nietemin is gemene pulmonale arterie druk 24.0 ± 7.7 mm Hg teen die maksimum kardiale indeks in die kontrole groep van 4.4 ± 1.1 l.min-1.m-2 tydens eenlongnarkose in die kontrole groep. Hierdie weerspieël dus ’n relatief beperkte verhoging in pulmonale arterie druk in vergelyking met die verhoging in pulmonale arterie druk wat gebeur het tydens die administrasie van dobutamien. Die waarskynlikste rede hoekom daar ’n beperkte verhoging in pulmonale arterie druk sou gewees het tydens die infusie van dobutamien is die afblaas effek van die nie-geventileerde long wat die verhoging in PA druk beperk het. Oksigenasie tydens eenlongnarkose Die volgende waarnemings is gemaak in verband met suurstof vloed, veneuse en arteriële oksigenasie tydens eenlongnarkose in die kontrole groep: 1. Die kombinasie van Induksie van narkose en die 1ºC vermindering in temperatuur het saamgegaan met ’n 40% vermindering in suurstof verbruik tydens twee long narkose. Hierdie vermindering in suurstof verbruik het voortgegaan tydens eenlongnarkose. 2. Die aanvang van eenlongnarkose is geassosieerd met ’n verhoging in kardiale omset in vergelyking met albei die basislyn eenlongnarkose en wakker state. 3. Die gevolge van punte 1 en 2 hierbo is dat die gemengde veneuse suurstof saturasie vanaf 75% en die gemeng veneuse suurstof spanning vanaf 5.4 kPa (toe die pasiënte wakker was) gestyg het tydens4. Tydens eenlongnarkose het die betekenisvolle verhoging in veneuse oksigenasie veroorsaak dat daar ’n verhoging in arteriële oksigenasie was in vergelyking met wanneer die pasiënte wakker was. Hierdie styging in arteriele oksigenasie was ten spyte van die 37% aftakking wat teenwoordig was tydens eenlongnarkose. 5. Onder toestande in die huidige studie, het dobutamien tydens eenlongnarkose nog arteriële nog veneuse oksigenasie verbeter nie, maar die arteriele oksigenasie het konstant gebly. ’n Belangrike observasie wat daarmee saamgaan is dat dobutamien toediening nie met ’n daling in arteriële suurstof spanning geassosieer is nie. Vervolgens, die hipotese dat die verhoging in kardiale omset geassosieer met dobutamien toediening tydens eenlongnarkose ’n verhoging in arteriële oksigenasie beweeg bring, is dus verwerp. Die verwerping van die hipotese van die deel van die studie beteken dat die bevindinge die teenoorgestelde is van die studies gepubliseer deur Mathru en sy kollegas en Nomoto en Kawamura. Hierdie outeurs het gedemonstreer dat die toediening van inotrope ’n verhoging in arteriële oksigenasie teweeg gebring het. Nietemin is die teenoorgestelde gevolgtrekkinge nie teenstrydig met mekaar nie. Inteendeel hierdie verskille help ons om die effek van ’n verhoging in kardiale omset of arteriële oksigenasie in die teenwoordigheid van ’n betekenisvolle aftakking duidelik te maak. Die verskille tussen die studies kan op die volgende manier verduidelik word. Toestande wat in die huidige studie teenwoordig was het veroorsaak dat die verband tussen suurstof lewering en verbruik baie hoog was en dat die gemeng veneuse suurstof spanning baie hoog was om mee te begin alvorens dobutamien geinfuseer is. Dus is die veneuse saturasies op die plat deel van albei die suurstof dissosiasie kurwe en ook van die verband tussen kardiale omset en arteriële suurstof inhoud oorspronklik deur Kelman, Nunn en kollegas beskryf. Verdere verhogings in kardiale omset sou dus nie verwag word, en het nie, verhogings in gemeng veneuse suurstof spanning, gemeng veneuse suurstof saturasie of gemeng veneuse suurstof inhoud teweeg gebring. Dus, arteriële suurstof inhoud en saturasie het nie verander na die verhoging in kardiale omset wat teweeg gebring is deur die toediening van dobutamien in die huidige studie. Inteendeel, in die studie deur Mathru en kollegas, is die lae aanvanklike veneuse saturasie en spanning verbeter deur verhogings in die verband tussen suurstoflewering en suurstofverbruik. Omdat die veneuse saturasie aan die begin van die Mathru studie laag was, is betekenisvolle voordeel in arterieël oksigenasie teweeg gebring deur om die kardiale omset te verhoog. ’n Groot bekommernis vir die klinikus is dat die aftakking mag verhoog met die toediening van die inotroop dobutamien tydens eenlongnarkose en, op die manier, arteriële oksigenasie mag verminder. Die invloed van dobutamien op arteriële oksigenasie tydens eenlongnarkose mag teoreties te wyte wees aan die balans van die volgende uiteenlopende faktore: 1. Deur om die verband tussen suurstof lewering en verbruik te verbeter, sal dobutamien gemeng veneuse suurstof spanning verhoog. Hierdie verhoging sal arteriële oksigenasie verbeter in die teenwoordigheid van ’n groot aftakking, 2. Die bogenoemde moet teenoor potensiële verhogings in suurstofverbruik deur dobutamien oorweeg word. Die gevolge hiervan sou potensieel ’n vermindering in gemeng veneuse suurstof spanning wees. Sulke verhogings in suurstof verbruik is nie tydens die huidige studie gesien nie,3. ’n Verhoging in pulmonale arterie druk wat saamgaan met die verhoogde kardiale omset sal hipoksiese pulmonale vasokonstriksie teenwerk wat die aftakking in albei die geventileerde en nie geventileerde longe sal verhoog, 4. Direkte inhibisie van hipoksiese pulmonale vasokonstriksie deur dobutamien en, 5. Die invloed van gemeng veneuse suurstof spanning op hipoksiese pulmonale vasokonstriksie moet ook oorweeg word (d.i. hoe gemeng veneuse suurstof parsiele druk sal hipoksiese pulmonale vasokonstriksie inhibeer). Nietemin, ten spyte van die bekommernisse rondom hipoksemie tydens die toediening van dobutamien tydens eenlongnarkose, het dobutamien toediening nie ’n verlaging in arteriële suurstof spanning teweeg gebring nie, en ook het dit nie die koste van oksigenasie verhoog nie. Verder, die bevindinge van studies tydens eenlongnarkose in die laterale decubitus posisie deur Mathru en sy kollegas, Nomota en Kawamura en ook die huidige studie, dui aan dat die toediening van lae dosisse van dobutamien nie toe ’n verhoging in aftakking lei nie. Inteendeel, die voordelige effekte van die verhoging in kardiale omset op veneuse saturasie het veroorsaak dat daar ’n verhoging in arteriële saturasie is in die studie deur Mathru en sy kollegas soortgelyke meganismes is waarskynlik ook van toepassing in die studie wat gedoen is deur Nomoto en Kawamura. Dus, dwars deur die literatuur, is daar geen huidiglike bewys dat die toediening van dobutamien tot en met dosisse van 7μg.kg-1.min-1 aftakking verhoog of arteriële oksigenasie versleg in mense onderworpe aan eenlongnarkose in die laterale decubitus posisie. Dit is duidelik dat die vasodilatoriese effekte van dobutamien wat moontlik ’n verhoging in aftakking fraksie teweeg kan bring, nie die enigste faktore is om te oorweeg wanneer die middel se invloed op arteriële oksigenasie bestudeer word nie. Dit is ook van kliniese belang om die invloed van inotrope middels op veneuse suurstof inhoud te oorweeg. Dit is moontlik dat ’n aftakking verhoog kan word deur die toediening van ’n inotroop. Nietemin, mag die negatiewe effek wat die toediening van ’n inotroop sal inhou op arteriële oksigenasie deur middel van sy verhoging in aftakking, negeer word indien veneuse oksigenasie voordelig beïnvloed is. Verder, indien die verhoging in veneuse oksigenasie wat teweeggebring word deur die toediening van inotrope baie betekenisvol is, mag die gevolg hiervan wees dat arteriële oksigenasie voordelig beïnvloed word soos die geval in die huidige studie was. Die huidige benadering waar die kwaliteit van die bloed wat deur die aftakking vloei die arteriële oksigenasie beïnvloed, skuif die klem van voorkoming en behandeling van hipoksemie tydens eenlongnarkose van die long na die toereikendheid van die sirkulasie. Met ander woorde, die klem is geskuif van wat gebeur in die nie-geventileerde long (hipoksie pulmonale vasokonstriksie) tot primêr die toereikendheid van suurstof flux tydens eenlongnarkose. Ekstrinsieke en intrinsieke PEEP tydens eenlongnarkose Die invloed van PEEP op hemodinamika en oksigenasie tydens eenlongnarkose in die huidige studie mag as volg opgesom word. Toe PEEP5 tydens eenlongnarkose toegedien is: 1. Nie regter ventrikulêre funksie, hemodinamika, suurstof flux nog arteriële oksigenasie is beïnvloed deur die toediening van PEEP5 in vergelyking met die stap wanneer geen eksterne PEEP toegedien is nie. 2. Betekenisvolle hoeveelhede intrinsieke PEEP is teenwoordig tydens eenlongnarkose in die kontrole groep.Die hoeveelheid intrinsieke PEEP wat teenwoordig was, is swak maar betekenisvol verwant aan die graad obstruktiewe lugwegsiekte wat teenwoordig was gemeet deur pre-operatiewe longfunksie toetse. 3. Die waarskynlikste rede hoekom PEEP5 nie ’n verskil gemaak het aan oksigenasie of hemodinamika nie is die teenwoordigheid van soortgelyke hoeveelhede intrinsieke PEEP tydens eenlongnarkose. Hierdie bevinding bevestig Myle’s se beweringe dat lae vlakke intrinsieke PEEP voordelige effekte op oksigenasie tydens eenlongnarkose mag hê. PEEP10 toediening aan die onderlong tydens eenlongnarkose in die huidige studie het tot ’n vermindering in slagvolume gelei. Hierdie vermindering is primêr veroorsaak deur ’n vermindering in voorlading en nie die gevolg van ’n verhoging in pulmonale vaskulêre weerstand nie. Die gevolgtrekking is gemaak omdat regerventrikulere enddiastoliese volume verlaag het maar pulmonale vaskulêre weerstand het nie verhoog tot vlakke wat bekend is om regter ventrikulêre funksie te belemmer nie. Die vermindering in die verhouding tussen suurstof lewering en suurstof verbruik wat geïnduseer is deur PEEP10 het (voorspelbaar) gemeng veneuse suurstof spanning verminder en kon potensieël gelei het tot belemmering in arteriële oksigenasie. Indien minder voordelige sirkulatoriese toestande geheers het tydens die huidige studie, sou groter (oorbodige) hoeveelhede PEEP slegter kardiorespiratoriese gevolge tot gevolg gehad het. Ter opsomming, optimalisering van die volume van die onderlong tydens eenlongnarkose speel ’n belangrike rol in die bepaling van arteriële oksigenasie. Nietemin, die terapeutiese indeks vir PEEP is nou en die narkotiseur het die behoefte om te weet wanneer die volume van die onderlong optimaal is. In die opsig, is ’n betekenisvolle probleem tydens eenlongnarkose dat meting van funksionele residuele kapasiteit nie huidiglik maklik is nie

Purpose: The aim of this study was to determine if the use of local anesthesia with general anesthesia results in less postoperative pain. The alternative hypothesis is that children will experience less postoperative discomfort when utilizing intraligamental local anesthetic during the intra-operative time period. Methods: Patients were recruited for this single blind, randomized, prospective cohort study with the following inclusion criteria: English speaking children age 3-6 years, ASA I/II requiring general anesthesia for dental treatment. Randomization was done to place patients in groups of no local anesthetic vs. local anesthetic administration. A Wong-Baker Faces Pain Scale was utilized to evaluate pre-operative and postoperative pain. Data were compared using a two way mixed model ANCOVA controlling for sex, ethnicity, pre-op pain, and intra-op meds given. Results: Data was collected and evaluated on 90 patients. There was a statistically significant difference in postoperative pain for patients who received extractions without local anesthesia vs. those with local anesthetic. There was no statistically significant difference in pain outcomes based solely on whether local anesthetic was administered regardless of treatment type. Conclusions: The outcome of this study shows evidence for provision of local anesthetic during general anesthesia in patients receiving extractions to reduce postoperative pain.

Purpose: The purpose of this study is to determine the impact that the introduction of articaine has had on local anesthetic selection by general and pediatric dentists for use in three different age groups of children.Methods: Using a cross sectional survey design, a questionnaire regarding the use of local anesthetics in children was mailed to a random sample of 500 general dentists from North Carolina, 500 general dentists from Virginia, and all 230 pediatric dentists from North Carolina and Virginia. The 16-item questionnaire included questions regarding the preferred local anesthetic to use in three different age groups, 2-3 years of age, 4-6 years of age, and 7-10 years of age. Furthermore, the questionnaire also included questions specifically on articaine use in the three different age groups and any related side effects. The association between dental practitioner type and anesthetic use was tested using chi-square or Fisher's exact test.Results: A sample of 337 dentists completed the questionnaire. There was no significant difference in preference of articaine except in older patients aged 7-10 years old where general dentists prefer articaine significantly more than do pediatric dentists (28.1% versus 15.9%). Lidocaine with epinephrine was the local anesthetic that was most preferred in all age groups by all practitioners. Pediatric dentists preferred lidocaine more often than general dentists and general dentists preferred lidocaine without epinephrine more often than pediatric dentists. Twenty-one percent of all dentists surveyed have used articaine in children under 4 years of age and 13% list articaine as the preferred local anesthetic for children under 4 years of age.Conclusion: While lidocaine with epinephrine is still the preferred local anesthetic for use in children, the use of articaine in children is very prevalent among general and pediatric dentists. Articaine use becomes more prevalent as the age of the patient increases and many pediatric and general dentists are using articaine in children under four years of age.

RESUMO Comparou-se os períodos de latência e duração da lidocaína 2% associada à adrenalina 1:100.000 (Lidocaína 100 ® da DFL), e da articaína 4% associada à adrenalina 1:200.000 (Septanest 1:200.000 ® da Septodont) e 1:100.000 (Septanest 1:100.000 ® da Septodont), na polpa dentária e gengiva vestibular, em anestesias locais infiltrativas maxilares. Vinte pacientes voluntários, saudáveis, de ambos os sexos, entre 18 e 50 anos de idade receberam tratamento restaurador de baixa complexidade ou selamento de cicatrículas e fissuras nas superfícies oclusais de três dentes superiores posteriores de uma mesma hemiarcada. Cada paciente recebeu, aleatoriamente, um tubete (1,8 ml) de cada solução anestésica local em três consultas. Os períodos de latência e duração da anestesia local na polpa dentária foram monitorados com um aparelho estimulador pulpar elétrico (Vitality Scanner Model 2005 ® da Analytic Endodontics) e na gengiva vestibular por meio do estímulo com a ponta de um explorador. Através do Teste de Kruskal-Wallis foram detectadas diferenças estatisticamente significantes ao nível de 5% entre lidocaína 2% associada à adrenalina 1:100.000, quando comparada tanto com a articaína 4% associada à adrenalina 1:200.000 quanto com a articaína 4% associada à adrenalina 1:100.000, para as variáveis: período de latência e duração na polpa dentária e período de duração na gengiva, sendo que a lidocaína 2% associada à adrenalina 1:100.000 apresentou a maior média para o período de latência pulpar e as menores médias para os períodos de duração na polpa dentária e na gengiva (respectivamente, 2,8, 39,2 e 42,2 minutos),quando comparada à articaína 4% associada à adrenalina 1:200.000 (respectivamente, 1,6, 56,7 e 55,3 minutos) e 1:100.000 (respectivamente, 1,4, 66,3 e 64,7 minutos). Houve diferença estatisticamente significante entre as duas soluções de articaína apenas para o período de duração na gengiva, cuja maior média foi a da articaína 4% associada à adrenalina 1:100.000. Não houve diferença estatisticamente significante entre os grupos para o período de latência gengival. Conclui-se que as soluções de articaína apresentam latência mais curta e duração mais longa do que a solução de lidocaína quando da anestesia pulpar. Para a latência gengival não há diferença entre as três soluções testadas, porém, para a duração gengival, a solução de articaína 4% associada à adrenalina 1:100.000 apresenta a maior duração. / SUMMARY Local anesthesias by maxillar infiltration with 2% lidocaine associated with 1:100.000 adrenalin (Lidocaina 100 ® by DFL), 4% articaine associated with 1:200.000 (Septanest 1:200.000 ® by Septodont) and 1:100.000 adrenalin (Septanest 1:100.000 ® by Septodont) were compared concerning to their onset and duration on dental pulp and gingiva. Twenty healthy volunteer patients, of both gender, between 18 and 50 years of age, received filling treatment of low complexity or fissure sealing on the occlusal surface of three superior posterior teeth of the same side. Each patient randomly received an ampoule (1,8ml) of each local anesthetic solution on three appointments. The onset and duration periods of local anesthesia on dental pulp were monitored with an electric pulptester (Vitality Scanner Model 2005 ® by Analytic Endodontics) and on buccal gingiva by the stimulus performed with the point of a probe. Kruskall-Wallis test identified statistic significant difference by the level of 5% between 2% lidocaine associated with 1:100.000 adrenalin when compared with both 4% articaine associated with 1:200.000 or 1:100.000 adrenalin for the following variants: onset and duration periods on dental pulp and duration period on gingiva. 2% lidocaine associated with 1:100.000 adrenalin presented the longest average for onset period on dental pulp and the minorest averages for duration periods on dental pulp and gingiva (respectively, 2,8, 39,2 and 42,2 minutes), when compared with 4% articaine associated with 1:200.000 (respectively, 1,6, 56,7 and 55,3 minutes) and 1:100.000 adrenalin (respectively, 1,4, 66,3 and 64,7 minutes). There was statistic significant difference between the two articaine solutions just for duration period on gingiva, whose longest average was that of 4% articaine associated with 1:100.000 adrenalin. There was no statistic significant difference between the groups for onset period on gingiva. It can be concluded that both articaine solutions present faster onset and longer duration than the lidocaine solution on pulpal anesthesia. For gingival onset there is no difference between the three tested solutions, however, for gingival duration, 4% articaine associated with 1:100.000 adrenalin presents the longest duration.

The testing of any physiological diagnostic system in-vivo depends critically on the stability of the anesthetized animal used. That is, if the systemic physiological parameters are not tightly controlled, it is exceedingly difficult to assess the precision and accuracy of the system or interpret the consequence of disease. In order to ensure that all measurements taken using the experimental system are not affected by fluctuations in physiological state, the animal must be maintained in a tightly controlled physiologic range. The main goal of this project was to develop a robust monitoring and control system capable of maintaining the physiological parameters of the anesthetized animal in a predetermined range, using the instrumentation already present in the laboratory, and based on the LabVIEWR software interface. A single user interface was developed that allowed for monitoring and control of key physiological parameters including body temperature (BT), mean arterial blood pressure (MAP) and end tidal CO2 (ETCO2). Embedded within this interface was a fuzzy logic based control system designed to mimic the decision making of an anesthetist. The system was tested by manipulating the blood pressure of a group of anesthetized animal subjects using bolus injections of epinephrine and continuous infusions of phenylephrine (a vasoconstrictor) and sodium nitroprusside (a vasodilator). This testing showed that the system was able to significantly reduce the deviation from the set pressure (as measured by the root mean square value) while under control in the hypotension condition (p < 0.10). Though both the short-term and hypertension testing showed no significant improvement, the control system did successfully manipulate the anesthetic percentage in response to changes in MAP. Though currently limited by the control variables being used, this system is an important first step towards a fully automated monitoring and control system and can be used as the basis for further research.