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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors sought to test whether a deviation existed for the correlation between anesthetic potency and the oil/gas partition coefficient at an extreme of lipid solubility. For thiomethoxyflurane, the sulfur analog of methoxyflurane, the oil/gas partition coefficient was 7230 +/- 50 SEM, and MAC (minimum alveolar concentration of thiomethoxyflurane required for anesthesia) in 4 dogs was 0.035 +/- 0.008 percent of 1 atm. This agrees with the potency predicted by the lipid solubility, although thiomethoxyflurane is 7 1/2 times more potent than methoxyflurane, to date the most potent available anesthetic. Thiomethoxyflurane water/gas and blood/gas partition coefficients were 5.4 +/- 0.3 and 68.1 +/- 1.5, respectively. The latter coefficient accords with the prolonged recovery associated with this agent. Renal and hepatic blood chemistries measured on the 1st and 7th days following anesthesia showed only small changes from preanesthetic values.
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PMID:Some characteristics of an exceptionally potent inhaled anesthetic: thiomethoxyflurane. 55 38

In 7 subjects, serial EEGs, serum bromide determinations, and psychological tests were done prior to and following 13.83 +/- 0.74 (SEM) MAC-hours of halothane anesthesia. Significant psychological impairment demonstrated 2 days following anesthesia in these subjects was absent 2 weeks following exposure to halothane. Nonspecific postanesthetic slowing of the EEG was found, qualitatively similar to but more marked than that following exposure to enflurane. Generalized EEG slowing, with a tendency toward posterior delta activity and significant reduction of frequency and amplitude of the alpha rhythm, persisted for 6 to 8 days following anesthesia. Rare sharp-wave activity developed in 3 subjects in the 1st week after halothane. A potentially psychoactive postanesthetic serum bromide level of 2.97 +/- 0.17 mEq/L (SEM) was found 5 days following anesthesia. Electroencephalographic changes characteristic of mild bromide intoxication were absent, suggesting that the psychological impairment noted after halothane anesthesia is probably not due to this metabolite; these psychological changes are probably due instead to persistence in the circulation of unchanged halothane.
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PMID:Electroencephalographic abnormalities following halothane anesthesia. 56 63

It has previously been demonstrated that an induction dose of thiopental, 25 mg/kg, without continuing anesthesia did not depress peripheral lung mucociliary clearance in the dog, whereas 2 hours of anesthesia with halothane, 1.2 MAC, did depress clearance. To determine whether this was because thiopental depresses the mucociliary apparatus less than halothane, this study compared mucociliary clearance after 2 hours of anesthesia with halothane with clearance after 2 hours of anesthesia with thiopental, 40 mg/kg. With thiopental, 40 mg/kg, 50% mucociliary clearance of tantalum from peripheral airways required 280 +/- 65 (SEM) minutes, which was comparable to clearance obtained with halothane, 1.2 MAC, 382 +/- 27 (SEM) minutes. Hence thiopental depresses mucociliary clearance as much as halothane does when both are administered in equivalent anesthetic doses for equal periods of time.
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PMID:Depression of lung mucociliary dlearance by thiopental and halothane. 57 63

Regional haemodynamic control by the cardiovascular baroreceptors was examined in dogs anaesthetized with 1 + MAC halothane in oxygen (1%). The open-loop relationships between carotid sinus pressure (CSP) and regional haemodynamics in the iliac, renal, mesenteric, aortic and coeliac beds were examined before vagotomy, following vagotomy and following thoracotomy. Around the carotid sinus reflex set point, the ratio of the reflex decrease in systemic arterial pressure to an increase in CSP (reflex gain) was -0.744+/-0.089 (mean+/-SEM): the latter increased to -1.275+/-0.093 following vagotomy. Reflex resistance changes were greatest in the renal bed and least in the coeliac bed, reflecting blood flow homeostasis which was well preserved in the renal bed but minimal in the coeliac bed. Thoracotomy in the dogs in which vagotomy had been performed resulted in no significant changes in the dependent variables studied. It is concluded that, in these dogs anaesthetized with 1 + MAC of halothane, baroreceptor control of regional pressure flow relationships is well preserved.
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PMID:Baroreceptor control of regional haemodynamics during halothane anaesthesia in the dog. 87 50

Rabbits have a high rate of ventilation which makes it difficult to obtain a sample of end-tidal gas by the usual procedures. An occlusion technique was developed which provided a gas sample equivalent to an end-tidal gas sample. MAC values were determined using this sampling method. The values obtained +/- SEM were: cyclopropane 15.6 +/- 1.7%, halothane 0.63 +/- 0.06% and ether 2.7 +/- 0.2%.
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PMID:Determination of MAC for halothane, cyclopropane and ether in the rabbit. 88 46

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in six dogs each with a tracheostomy, awake and during anaesthesia with halothane, enflurane and isoflurane (1-2.5 MAC). Isocapnic hypoxic ventilatory response (HVR) was expressed as the parameter A, such that the greater the value of A, the greater the hypoxic response. In the anaesthetized dogs HVR (A) was reduced significantly from the awake value of 2010 +/- 172 (mean + SEM) to 630 +/- 173 by 1 MAC halothane, 495 +/- 105 by 1 MAC enflurane and 952 +/- 157 by 1 MAC isoflurane (PL0.05). All three anaesthetic agents produced significant depression of HUR at 1 MAC, but enflurane was more depressant than isoflurane. At 1.5 MAC all three anaesthetics produced equal and significant depression of HVR at equianalgesic concentrations. Further increases in anaesthetic concentration caused no increase in depression. Hypercapnic drive, as measured by the slope of the VE/PACO2 response curve, was reduced significantly from 9.75 litre min-1 kPa-1 +/- 2.4 in awake dogs to 0.83 +/- 0.56 after 1 MAC halothane, 0.68 +/- 0.53 after 1 MAC enflurane and 1.58 +/- 0.75 after 1 MAC isoflurane. In addition, hypercapnia-induced augmentation of the hypoxic drive was abolished by 1 MAC halothane or enflurane and diminished markedly by 1 MAC isoflurane. It may be clinically significant that hypoxia and hypercapnia during anaesthesia with these agents did not produce optimal stimulation of ventilation.
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PMID:Depression of hypoxic ventilatory response by halothane, enflurane and isoflurane in dogs. 92 74

We studied recovery in 25 adult patients, ASA I, undergoing elective orthopaedic procedures after anaesthesia with 0.65 MAC desflurane (n = 16) or isoflurane (n = 9) with 60% nitrous oxide in oxygen. Early emergence from anaesthesia was assessed in the operating room by measuring time to spontaneous movement, cough, response to painful pinch, tracheal extubation, opening of the eyes and stating correct age, name and body parts. The return of cognitive functions in the late recovery phase was assessed in the post-anaesthesia care unit (PACU) by post-anaesthesia recovery scores (PARS), the Trieger dot test (TDT), and the digit substitution test (DST). In the early recovery phase, time to tracheal extubation, opening eyes, telling correct name, age and body parts occurred significantly faster in the desflurane group than in the isoflurane group (P < 0.05). The mean "triple orientation" time (to name, age, body parts) was 10.9 (SEM 0.9) min for desflurane, compared with 18.6 (2.5) min for isoflurane (P < 0.01). In the late recovery phase, desflurane patients had significantly greater PARS, more correct responses to the DST and fewer error responses to the TDT. Recovery times were not increased by increased duration of desflurane anaesthesia. The desflurane patients showed no delirium, minimal sedation and less shivering during the entire postoperative course. We conclude that desflurane anaesthesia was superior to isoflurane anaesthesia, not only in emergence, but also in the recovery of cognitive functions.
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PMID:Recovery of cognitive functions after anaesthesia with desflurane or isoflurane and nitrous oxide. 138 42

This study compared systemic hemodynamic and organ blood flow responses to equipotent concentrations of halothane and sevoflurane during spontaneous ventilation in the rat. The MAC values for halothane and sevoflurane were determined. Cardiac output and organ blood flows were measured using radiolabeled microspheres. Measurements were obtained in awake rats (control values) and at 1.0 MAC halothane or sevoflurane. The MAC values (mean +/- SEM) for halothane and sevoflurane were 1.10% +/- 0.05% and 2.40% +/- 0.05%, respectively. The PaCO2 increased to a similar extent in both groups compared with control values. During halothane anesthesia, heart rate decreased by 12% (P < 0.01), cardiac index by 26% (P < 0.01), and mean arterial blood pressure by 18% (P < 0.01) compared with control values. Stroke volume index and systemic vascular resistance did not change. During sevoflurane anesthesia, hemodynamic variables remained unchanged compared with control values. Coronary blood flow decreased by 21% (P < 0.01) and renal blood flow by 18% (P < 0.01) at 1.0 MAC halothane, whereas both remained unchanged at 1.0 MAC sevoflurane. Cerebral blood flow increased to a greater extent with halothane (63%; P < 0.01) than with sevoflurane (35%; P < 0.05). During halothane anesthesia, hepatic arterial blood flow increased by 48% (P < 0.01), whereas portal tributary blood flow decreased by 28% (P < 0.01). During sevoflurane anesthesia, hepatic arterial blood flow increased by 70% (P < 0.01) without a concomitant reduction in portal tributary blood flow. Total liver blood flow decreased only with halothane (16%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and organ blood flow responses to halothane and sevoflurane anesthesia during spontaneous ventilation. 144 79

Although general anesthesia frequently is used for eye surgery or used in experimental studies of circulation in the eye, few data are available describing its effects on ocular blood flow. The blood supply to the retina in humans and other mammals is derived from a dual circulation; the retinal vessels supply the inner neural layers while the choroidal vessels supply the outer retina. Both circulations are required for normal retinal function. Using radioactively labeled 15-microns microspheres containing Ce141, Sn113, or Nb95, blood flow was measured in the retina and choroid in cats (whose ocular circulation is similar to that of humans) and cerebral cortex during halothane anesthesia. In ten adult cats, retinal blood flow was 37 +/- 3, 54 +/- 6, and 59 +/- 4 ml.100 g-1.min-1 (mean +/- SEM) at 0.5, 1.0, and 1.5 MAC halothane, respectively, and corresponding values for cerebral cortical blood flow were 60 +/- 5, 69 +/- 6, and 98 +/- 14 ml.100 g-1.min-1 (mean +/- SEM), respectively. For both retinal and cerebral blood flows, values obtained at 1.0 and 1.5 MAC were significantly greater than those at 0.5 MAC (P less than 0.0167). In contrast to the effects on retinal blood flow, choroidal blood flow was significantly decreased during halothane anesthesia. Choroidal blood flow was 1,801 +/- 222, 1,309 +/- 167, and 1,091 +/- 126 ml.100 g-1.min-1 (mean +/- SEM) at 0.5, 1.0, and 1.5 MAC, respectively. Values obtained at 1.0 and 1.5 MAC differed significantly from those at 0.5 MAC (P less than 0.0167).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of halothane on retinal and choroidal blood flow in cats. 153 58

To determine the systemic haemodynamic and organ blood flow responses to the administration of sevoflurane during spontaneous ventilation, heart rate, cardiac index, mean arterial pressure, arterial blood gases, and blood flows to the brain, spinal cord, heart, kidneys and splanchnic organs were measured awake (control values) and after 30 min of anaesthesia with 0.5, 1.0, 1.2 or 1.5 MAC sevoflurane in rats. Cardiac output and organ blood flows were measured using radiolabelled microspheres. The MAC (mean +/- SEM) of sevoflurane was found to be 2.30 +/- 0.05%. At each concentration, haemodynamic variables were similar to awake values with the exception of a 12% reduction in mean arterial pressure at 1.5 MAC (P less than 0.01). Arterial PCO2 increased in a dose-related fashion. Cerebral and spinal cord blood flows increased at 1.2 and 1.5 MAC whereas coronary and renal blood flows did not change significantly. Portal tributary blood flow and preportal vascular resistance were unaffected. Hepatic arterial flow increased by 63% at 1.5 MAC (P less than 0.05) but total liver blood flow remained unchanged compared with awake values. In conclusion, the administration of sevoflurane during spontaneous ventilation produces a high degree of cardiovascular stability and maintains blood flow to major organs in the rat.
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PMID:Haemodynamic and organ blood flow responses to sevoflurane during spontaneous ventilation in the rat: a dose-response study. 155 Nov 49


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