Investigators have shown that monitoring the electrical activity of the brain can indicate CNS status and that it can enhance the assessment of anesthetic depth when used with other clinical signs. It is important to understand the variables that are produced by EEG monitors and used to assess CNS status and to understand similarities and differences between stages of intra-operative sleep. This investigation used well studied stages of normal sleep for comparison with different stages of intra-operativesleep. EEG data from 6 intra-operative from 6 intra-operative and 6 normal sleep subjects were collected on FM recorder and processed with 2 clinical EEG monitors. The results failed to show any similarities in EEG variables between stages of normal sleep and intra-operative sleep. Comparison of the two monitors in assessing similar EEG waveforms showed that they have different sensitivities to frequency and amplitude and they produce different results with differences in their ability to separate information.

Thesis (M.Sc.)--University of the Witwatersrand, Faculty of Science, 1968.

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Anesthesia, a state of being absent of sensation and consciousness, has been recognized since antiquity. Even today anesthesia is still best characterized by the lack of consciousness and sensations. Since anesthetic potency is correlated with lipid solubility, the site of action of general anesthetics has been thought to be hydrophobic in nature and to involve excitable membranes critical for interneuronal communications. Thus, general anesthetics may interact directly with functionally-relevant membrane proteins (via hydrophobic pockets) or indirectly, with the lipids surrounding these proteins. To better understand the details of general anesthetic action, I examined how halothane interacts with a functional synaptic protein, the acetylcholine receptor channel embedded in the membranes of cultured Xenopus myocytes. Next, I examined how changing the lipid composition, of these membranes, affected this interaction. Using the extracellular patch-clamp technique, I found that halothane, at clinically-relevant concentrations, shortened the burst duration of single receptor channels without affecting their conductance. Moreover, the halothane-induced reduction of burst durations was significantly attenuated after pretreatment with cholesterol-rich lipsomes which increased significantly the cholesterol content of these cells. These findings provide the first direct support for the role of membrane lipids in the mechanism of GA action. In particular, I demonstrated that increases in membrane cholesterol antagonize the anesthetic action of halothane. Although direct action of cholesterol on synaptic proteins cannot be ruled out, my data strongly suggest that membrane lipids are involved at a critical, but as yet undefined, site with which GAs interact. The exact manner by which increases in membrane cholesterol antagonize GA action remains to be eludicated.

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Bibliography: p. 207-236. / 236 p. : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This thesis examines the systemic and cerebral pharmacokinetics and pharmacodynamics of propofol following rapid administration, using regional pharmacokinetic techniques in a sheep preparation. New methods for measurement of cerebral blood flow, cerebral metabolic rate and depth of anaesthesia are developed and validated. The final studies show that distribution of propofol to the brain is dependent on cardiac output. / Thesis (Ph.D.)--University of Adelaide, Dept. of Anaesthesia and Intensive Care, 1997?

Made available in DSpace on 2014-11-10T11:09:37Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-02-14Bitstream added on 2014-11-10T11:58:10Z : No. of bitstreams: 1 000790332.pdf: 1313377 bytes, checksum: 1972edfbb043cd5b04104c3173943b63 (MD5) / O reconhecimento e o tratamento precoce da hemorragia intraoperatória é primordial para prevenir a morbidade e a mortalidade associada à perda aguda de volume circulante. Por outro lado, dexmedetomidina é um fármaco adjuvante da anestesia que, devido a sua ação vasoconstritora, poderia agravar estados de hipoperfusão regional associados à perda volêmica aguda. Objetivou-se avaliar os efeitos da infusão intravenosa contínua de dexmedetomidina associada à atropina sobre os índices globais de perfusão e sobre outras variáveis hemodinâmicas em cães anestesiados com isoflurano submetidos à hemorragia guiada a volume seguida pela reposição volêmica com sangue autólogo. Oito cães hígidos (19,5-29,2 kg) foram anestesiados em duas ocasiões com concentrações equipotentes (1,3 concentração alveolar mínima) de isoflurano administrado isoladamente (tratamento ISO) ou em associação com a dexmedetomidina intravenosa (bolus de 1,6 μg/kg, seguido por 2 μg/kg/h) (tratamento ISO-DEX) em um delineamento aleatório cruzado, aguardando-se 2 semanas de intervalo entre os tratamentos. A atropina (0,03 mg/kg, IM e 0,01 mg/kg, IV) foi administrada 30 minutos antes da hemorragia no tratamento ISO-DEX. A anestesia foi mantida em ambos os tratamentos sob ventilação com volume controlado (volume corrente: 12 mL/kg, pressão positiva no final de expiração: 7 cm H2O, frequência respiratória: 16-20 mov/min) com bloqueio neuromuscular produzido pelo atracúrio. Após a obtenção dos parâmetros pré-hemorragia (basal), foram retirados 10, 20, e 30% do volume sanguíneo total estimado (80 mL/kg) de forma progressiva, seguido por reposição volêmica com sangue autólogo nas mesmas proporções. Comparativamente ao valor basal, a hemorragia reduziu significativamente (p < 0,05) o índice de transporte de O2 (IDO2) e a saturação venosa mista (SvO2) em ambos os tratamentos. Embora a taxa de extração de O2 (TeO2) tenha se elevado ... / Early recognition and treatment of acute intraoperative hemorrhage is seminal for preventing the morbidity and mortality associated with circulating volume losses. On the other hand, dexmedetomidine is an adjuvant anesthetic drug that might aggravate global tissue hypoperfusion induced by acute hemorrage because of its vasopressor effects. This study aimed to evaluate the effects of a constant rate infusion of dexmedetomidine combined with atropine on global perfusion indexes and on other hemodynamic parameters in isoflurane anesthestized dogs that underwent a volume-guided hemorrhage model followed by volume replacement with autologous blood. Eight healthy dogs (19-30 kg) were anesthetized in two occasions with equipotent concentrations (1.3 minimum alveolar concentration) of isoflurne alone (treatment ISO) or isoflurane combined with dexmedetomidine (1.6 μg/kg bolus, followed by 2 μg/kg/h) (treatment ISO-DEX) in a randomized crossover design, allowing 2-week intervals between treatments. Atropine (0,03 mg/kg, IM and 0.01 mg/kg IV) was administered 30 minutes prior to hemorrhage in the dexmedetomidne treatment. Anesthesia was maintained in both treatments under neuromuscular blockade induced by atracurium and volume controlled ventilation (expired tidal volume: 12 mL/kg, positive end-expiratory pressure: 7 cm H2O, respiratory rate: 16-20 mov/min). After recording pre-hemorrhage data (baseline), stepwise withdrawal of 10, 20, and 30% of the estimated blood volume (80 mL/kg) was followed by volume replacement with autologous blood in the same proportion. When compared with baseline values, hemorrhage significantly (P < 0,05) reduced oxygen delivery índex (IDO2) and mixed-venous saturation (SvO2) in both treatments. Although the oxygen extraction ratio (O2ER) was increased (P < 0.05) from baseline during hemorrhage, the anaerobic threshold (point where the oxygen comsumption (IVO2) becomes dependent on the IDO2] was not reached in both ...