Mak Man Ting. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 116-125). / ABSTRACT --- p.i / ACKNOWLEDGMENTS --- p.iv / TABLE OF CONTENTS --- p.v / LIST OF TABLES --- p.ix / LIST OF FIGURES --- p.x / Chapter CHAPTER1 --- INTRODUCTION --- p.1 / Chapter CHAPTER2 --- LITERATURE REVIEW / Chapter 2.1 --- General Review on Crustacean Circulatory System --- p.3 / Chapter 2.1.1 --- General anatomy and function --- p.3 / Chapter 2.1.2 --- Control mechanisms of cardiac function --- p.5 / Chapter 2.1.2.1 --- Intrinsic control --- p.6 / Chapter 2.1.2.2 --- Extrinsic control --- p.6 / Chapter 2.1.3 --- Ontogenic changes in cardiac function --- p.8 / Chapter 2.1.3.1 --- Change in heart rate during development --- p.8 / Chapter 2.1.3.2 --- Change from myogenic heart to neurogenic heart --- p.9 / Chapter 2.2 --- Effect of Temperature on Crustacean Cardiac Function --- p.10 / Chapter 2.2.1 --- General effect of temperature on crustaceans --- p.10 / Chapter 2.2.2 --- Effect of temperature on heart rate --- p.11 / Chapter 2.2.3 --- "Inter-relationship between heart rate, stroke volume and cardiac output" --- p.14 / Chapter 2.2.4 --- Control mechanisms on crustacean cardiac function in response to temperature change --- p.15 / Chapter 2.3 --- Effect of Salinity on Crustacean Cardiac Function --- p.18 / Chapter 2.3.1 --- General effect of salinity on crustaceans --- p.18 / Chapter 2.3.2 --- Effect of salinity on heart rate --- p.21 / Chapter 2.3.3 --- Effect of salinity on hemolymph flow distribution --- p.25 / Chapter CHAPTER3 --- CHANGES IN HEART RATE DURING DEVELOPMENT / Chapter 3.1 --- Introduction --- p.27 / Chapter 3.2 --- Materials and Methods --- p.29 / Chapter 3.3 --- Results --- p.31 / Chapter 3.4 --- Discussion --- p.34 / Chapter CHATPER4 --- EFFECT OF SALINITY ON HEART RATE OF METAPENAEUS ENSIS / Chapter 4.1 --- Introduction --- p.43 / Chapter 4.2 --- Materials and Methods --- p.45 / Chapter 4.3 --- Results --- p.48 / Chapter 4.4 --- Discussion --- p.51 / Chapter CHATPER5 --- EFFECT OF TEMPERATURE ON HEART RATE OF METAPENAEUS ENSIS / Chapter 5.1 --- Introduction --- p.58 / Chapter 5.2 --- Materials and Methods --- p.59 / Chapter 5.3 --- Results --- p.62 / Chapter 5.4 --- Discussion --- p.77 / Chapter CHAPTER6 --- DEVELOPMENT OF HEART INNERVATION IN METAPENAEUS ENSIS / Chapter 6.1 --- Introduction --- p.86 / Chapter 6.2 --- Materials and Methods --- p.87 / Chapter 6.3 --- Results --- p.89 / Chapter 6.4 --- Discussion --- p.109 / Chapter CHAPTER7 --- CONCLUSIONS --- p.112 / REFERENCES --- p.116

No description available.

Chow Tsun Cheung, Louis. / "May 2000." / Thesis (M.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references. / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

The effects on the cardiac cycle length of stimulating the vagus nerves with single supramaximal electrical shocks depended upon when they were stimulated during the cycle. A maximum prolongation of the cardiac cycle was obtained when the vagi were stimulated 167 msec (SD±64) after the peak of an electrocardiogram P wave. The interval between a P wave and the subsequent vagal stimulation was called Pl-St interval. Pl-St(max) was the Pl-St interval at which maximum prolongation of the cardiac cycle occurred. Pl-St(max) increased significantly (p (0.001) with longer cardiac cycles. When the Pl-St intervals were shorter or longer than 167 msec (SD±64) the effects of vagal stimulation were less. The latent period for the effects of vagal stimulation was 195 msec (SD±32) The latent period also increased significantly (p(O.Ol) with longer cardiac cycles. The rise time of the vagal effect, obtained by subtracting (Pl-St(max)+ latent period) from the control cardiac cycle length, was 124 msec (SD+31) and occurred between Pl-St intervals of 167 msec (SD±64) and 291 msec (SD±70). The rise time did not vary with cardiac cycle length (p) 0.1), but the magnitude of the maximum response to vagal stimulation was inversely proportional to rise time (p <. 0.02). The peak response to vagal stimulation must have occurred when the vagal effects pegan somewhere in the middle of diastolic depolarization of the pacemaker cells in the S-A node. The reasons for this were discussed. The half-decay time for the effects of vagal stimulation was 210 msec (SD±102). The slope of the curve relating the prolongation of the cardiac cycle length to Pl-St is positive at Pl-St intervals less than 167 msec (SD±64) and negative at Pl-St intervals between 167 msec (SD±64) and 291 msec (SD±90). The positive slope ranged from 0.13 to 0.48 with a mean of 0.23. The paradoxical responses of the S-A node to vagal inhibitory input obtained by Reid (1969), Levy et al (1969)and Dong and Reitz (1970) would be explained by the dependence of the cardiac cycle length upon the time of arrival of vagal stimulus in relation to the previous P wave and upon the slope of the curve relating the prolongation of the cardiac cycle length to Pl-St interval being positive and between zero and two at Pl-St intervals less than 167 msec (SD±64. The effects of single shock stimulation of the vagus nerves persisted for 3.890 sec (SD+l.255)7 the number of cardiac cycles involved varied between 5 and 11. The duration of the effects of vagal stimulation did not depend upon when during the cardiac cycle the vagi were stimulated. A "dip" in the response to vagal stimulation was present in all the experiments. The possibility of the "dip" phenomenon being due to simultaneous stimulation of the sympathetic fibres in the vago-sympathetic trunk was ruled out. It is suggested that the "dip" phenomenon may be due to transient accumulation of K+ in the interstitial fluid surrounding the pacemaker cells in the S-A node.There was no paradoxical response of the smooth muscle in the distal colon of the adult rabbit when the frequency of sympathetic inhibitory input was continuously increased. A paradoxical response in the frequency but not in the size of the contraction of the smooth muscle was obtained when the sympathetic nerves were stimulated with bursts of stimuli, each burst consisting of 5-40 impulses, 10 msec apart. One may conclude from this that the delay of the next spontaneous contraction but not the inhibition of the size of smooth muscle contraction is dependent upon the arrival time of a burst of stimuli during a contraction cycle. This was confirmed in an experiment when the sympathetic nerves were stimulated with single bursts of stimuli applied at different times during the contraction cycle. It is unlikely that such a paradoxical response would occur under physiological conditions as this would require the natural sympathetic efferent discharges to the smooth muscle to occur in regular bursts, each burst consisting of impulses at a high frequency. Stimulation of the sympathetic nerves at 3, 5, 10 and 25 PPS caused an inhibition of the size and frequency of smooth muscle contraction in the distal colon of the newborn rabbit. Assuming that the cholinergic fibres are excitatory there is therefore no evidence for the sympathetic fibres to the distal colon being cholinergic in the newborn rabbit. This is contrary to Burn's (1968) report of the sympathetic fibres being motor and cholinergic to the small intestinal smooth muscle in the newborn rabbit.The heart rate increased rapidly at the onset of exercise and then more gradually over the rest of the exercise period. The initial increase in the heart rate during exercise was not affected by adrenergic blockade but the subsequent increase in heart rate was significantly reduced by adrenergic blockade. Hence the increase in heart rate at the onset of exercise is due primarily to a decrease in the cardiac vagal efferent discharge, whereas the subsequent increase in heart rate is due to both a further decrease ln vagal discharge and an increase in sympathetic discharge to the S-A node. In almost all the sub jects there was initially a rapid decline in the heart rate in the post-exercise period, but subsequently the heart rate returned to resting levels in a variety of ways. These were classified into 5 types. Of particular interest to the present study was the Type V pattern of heart rate change. This was characterised by an increase in heart rate of 6 beats or more per minute during the post-exercise period, with or without superimposed arrhythmia. The Type V pattern may be the equivalent of the paradoxical responses to inhibitory input demonstrated in animal experiments i.e. an increase in the heart rate with increasing vagal stimulation frequency. Type V pattern occurred more frequently at mild exercise levels (4 out of 14) than at moderate exercise level (lout of 14) and also more frequently in adrenergic blocked individuals (11 out of 28) than in control subjects (5 out of 28) It is suggested that the sympathetic effects on the P-R interval and arterial baroreceptor modulation of vagal efferent discharge protect again st the occurrence of paradoxical responses to vagal inhibitory input. They may do so by confining the vagal discharge to the rise time of vagal effect during the cardiac cycle. On the other hand the Type V pattern in p-adrenergic blocked individuals may be due to a decrease in the vagal discharge, in which case Type V pattern would not be a paradoxical response. The changes in minute ventilation in the post-exercise period were also variable. Besides a gradual decline in minute ventilation there were also gradual increases and sudden increases and decreases in minute ventilation. These may represent a form of paradoxical response to increasing inhibitory input and decreasing excitatory input to the respiratory neurones in man. However, all the changes in minute ventilation could also be explained by fluctuating excitatory and inhibitory neural input to the respiratory neurones. / Thesis (MD)-University of Natal, Durban, 1973.

Thesis (Ph. D.)--University of Hawaii at Manoa, 1982. / Bibliography: leaves 260-277. / Microfiche. / xiv, 277 leaves, bound ill. 29 cm

Graduation date: 1993

Behavioral and physiological reactivity, and its relationship to cardiovascular disease has been studied in men for a number of years, and the expression of anger has been identified as a possible contributing factor. Few studies, however, have focused specifically on the reactivity of women, and those which have suggest that women are less reactive to laboratory tasks than men. For the present study, 45 undergraduate women, ages 19-21 were selected from a larger sample of 135 women to represent three discrete groups: (1) low anger/low denial, (2) high anger/low denial, and (3) low anger/high denial, based on their scores on the State-Trait Anger Expression Inventory, P and the Marlowe-Crowne Social Desirability Scale. It was hypothesized that the three groups would show reliable differences in heart rate and blood pressure during presentation of a stressful laboratory stimulus, the Stroop Color and Word Test. Each subject received three counterbalanced conditions: (1) no feedback, (2) error feedback without observer present, (3) error feedback with observer present. As hypothesized, women who reported a high level of denial and a low level of anger exhibited reliably greater systolic blood pressure to the no-feedback condition than subjects who reported low levels of denial and anger. The hypothesis that all groups would display greater A reactivity in a condition which provided error feedback with observation was not supported. / Master of Science

Intrakardinė nervų sistema atlieka svarbų vaidmenį reguliuodama širdies ritmą, miokardo laidumą ir susitraukimo jėgą bei vainikinių arterijų tonusą. Neišnešiotų kūdikių intrakardinės inervacijos topografija yra svarbi, atliekant perkateterinę radijodažninę abliaciją, taikomą medikamentiniam gydimui rezistentiškų supraventrikulinių bei atrioventrikulinių reciprokinių tachikardijų atvejais. Tyrėjų duomenys, apie mazgų topografiją bei struktūrinę organizaciją, yra gana skirtingi ir, kad žmogaus vaisių širdies intrakardinis nervinis rezginys iš tiesų nėra pakankamai ištirtas. Todėl darbo tikslas buvo ištirti žmogaus epikardinių nervinių mazgų topografiją ir morfologij�� įvairaus amžiaus vaisių širdyse. Disertacinio darbo rezultatai rodo, kad (1) žmogaus epikardiniai nerviniai mazgai yra lokalizuoti definityvinėse vietose jau penkiolikos savaičių vaisiaus širdyje; (2) epikardinių mazgų skaičius ir pasklidimas žmogaus 15-40 savaičių vaisiuose nėra susijęs su amžiumi; (3) epikardinių nervinių subrezginių mazgų laukų topografija yra pastovi tirtose vaisių širdyse; (4) epikardinių nervinių subrezginių mazgų laukų struktūra – ganglijų skaičius ir jų sritinė lokalizacija yra individualiai kintantys; (5) epikardinių mazgų ir mazginių neuronų dydis, o taip pat mazgų forma bei tarpmazginių nervų skaičius yra susiję su vaisių amžiumi. / Intrinsic cardiac nervous system plays a crucial role in regulation of heart rate, contractility and tone of the coronary vessels. In neonates and infants, the intrinsic neural pathways are considered to be important for radiofrequency ablation that is performed in cases of incessant supraventricular and atrioventricular nodal reentrant tachycardia. Findings regarding to topography of intrinsic cardiac ganglia in the human fetuses differ substantially and deserves a further examination. The aim of this study was to investigate the topography and morphology of the human epicardiac neural ganglia during prenatal period. Results of the present study show, that: (1) the human fetal epicardiac ganglia are in their definitive location already from 15 weeks of gestation; (2) the number of the fetal epicardiac ganglia does not age-dependent and does not differ significantly between the fetal and the adult humans; (3) the distribution of the fetal epicardiac ganglia does not age-dependent; (4) the variability of the neural ganglionated fields, including both the ganglion number and the regional ganglion density, vary substantially from heart to heart; (5) the sizes of epicardiac ganglia in the human fetuses differ substantially from the adult ones, and that the ganglion structure, ganglion size and the number of interganglionic nerves are dependent on gestation stage of the human fetuses.

No abstract available. / Thesis (M.D.)-University of Natal, 1973.

Indiana University-Purdue University Indianapolis (IUPUI) / Autonomic innervation of the heart begins in utero and continues during the neonatal phase of life. A balance between the sympathetic and parasympathetic arms of the autonomic nervous system is required to regulate heart rate as well as the force of each contraction. Our lab studies the development of sympathetic innervation of the early postnatal heart in a conditional knockout (cKO) of Src homology protein tyrosine phosphatase 2 (Shp2). Shp2 is a ubiquitously expressed non-receptor phosphatase involved in a variety of cellular functions including survival, proliferation, and differentiation. We targeted Shp2 in post-migratory neural crest (NC) lineages using our novel Periostin-Cre. This resulted in a fully penetrant mouse model of diminished cardiac sympathetic innervation and concomitant bradycardia that progressively worsen. Shp2 is thought to mediate its basic cellular functions through a plethora of signaling cascades including extracellular signal-regulated kinases (ERK) 1 and 2. We hypothesize that abrogation of downstream ERK1/2 signaling in NC lineages is primarily responsible for the failed sympathetic innervation phenotype observed in our mouse model. Shp2 cKOs are indistinguishable from control littermates at birth and exhibit no gross structural cardiac anomalies; however, in vivo electrocardiogram (ECG) characterization revealed sinus bradycardia that develops as the Shp2 cKO ages. Significantly, 100% of Shp2 cKOs die within 3 weeks after birth. Characterization of the expression pattern of the sympathetic nerve marker tyrosine hydroxylase (TH) revealed a loss of functional sympathetic ganglionic neurons and reduction of cardiac sympathetic axon density in Shp2 cKOs. Shp2 cKOs exhibit lineage-specific suppression of activated pERK1/2 signaling, but not of other downstream targets of Shp2 such as pAKT (phosphorylated-Protein kinase B). Interestingly, restoration of pERK signaling via lineage-specific expression of constitutively active MEK1 (Mitogen-activated protein kinase kinase1) rescued TH-positive cardiac innervation as well as heart rate. These data suggest that the diminished sympathetic cardiac innervation and the resulting ECG abnormalities are a result of decreased pERK signaling in post-migratory NC lineages.