ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Acetylcholine and choline concentrations in brain structures of rats during anesthesia with halothane (0.7-1.0 per cent inspired), enflurane (2.7-3.0 per cent, inspired) and ketamine (40 mg/kg, iv) were measured by gas chromatography. The turnover rate (biosynthesis) of acetylcholinein vivowas estimated by infusing phosphoryl(Me-14C)choline intravenously, determining specific activities of choline and acetylcholine, and applying principles of steady-state kinetics to compute the fractional rate constant of acetylcholine. Acetylcholine concentrations in brain structures did not change during anesthesia. Halothane decreased the acetylcholine turnover rates in all parts of the brain. Enflurane decreased the acetylcholine turnover rate in the cerebral cortex only, but not in the caudate nucleus, the hippocampus, and the hypothalamic and thalamic regions. During anesthesia with ketamine, acetylcholine turnover rates were reduced in the caudate nucleus and the hippocampus, but not in the cerebral cortex and the hypothalamic and thalamic regions. The results suggest that acetylcholine turnover rate and utilization are related to anesthetic-induced electrophysiologic changes in cortical and subcortical structures.

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

An animal model was used to investigate the comparative fetal toxicities of three inhalational anesthetics. Pregnant Sprague-Dawley rats were exposed for eight hours a day throughout the 21 days of gestation to graded concentrations of halothane (0.16-0.32 per cent), or nitrous oxide (1-50 per cent), or a nitrous oxide (10 per cent) and halothane (0.16 per cent) mixture, or methoxyflurane (0.01-0.08 per cent). High subanesthetic concentrations of all the inhalational anesthetics could cause fetal growth retardation (e.g., 3-21 per cent decreases in normal fetal weights), but this was unaccompanied by significant fetal loss (overall rate: 4.8 ±1.2 per cent, mean ± SE, in anesthetic groups) or any evidence of skeletal or gross abnormalities related to treatment. It is concluded that these rodent studies do not implicate any specific inhalational anesthetic agent in fetal toxicity, and that the effects of additional factors, such as stress, must be considered.

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

This study was designed to determine whether the isolated rat hepatocyte preparation could be used to assess the comparative toxicities of halothane, methoxyflurane, enflurane and chloroform. Suspensions of rat hepatocytes, prepared by a collagenase-based isolation technique, were incubated for 20 or 60 minutes in the presence of various concentrations of these anesthetics. Toxicity was assessed by measuring the leakage of intracellular potassium ions and alanine aminotransferase, decrease in the rate of ureogenesis, and increase in the lactate: pyruvate ratio. Toxicity measured after 20 minutes of incubation was dose-related, and the magnitudes of the effects of chloroform and methoxyflurane were approximately equal, and significantly P<0.01) exceeded that of halothane. Enflurane did not affect potassium ion or alanine aminotransferase release, even after 60 minutes of incubation, at which time halothane toxicity was markedly increased (P<0.002). Enflurane did produce effects on ureogenesis and the lactate:pyruvate ratio, although these were less than those of the other agents. These data suggest that the toxic effects of halogenated volatile anesthetics measured in thisin-vitropreparation are of the same comparative order as their clinical hepatotoxic potentials.

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

The hemodynamic interaction of acute hypovolemia and halothane anesthesia in dogs with increased intra-abdominal pressure caused by intraperitoneal instillation of N2, N2O and CO2was studied. During normovolemia and just basal pentobarbital anesthesia, the response to increase of intra-abdominal pressure to 40 torr consisted of a 35 per cent decrease in cardiac output, which was equal to the decrease in magnitude of inferior vena caval blood flow. During basal pentobarbital anesthesia, the addition of halothane anesthesia (1 MAC) in combination with hypovolemia (15 per cent blood volume loss) depressed the pre-inflation cardiac output more than addition of halothane anesthesia alone or induction of hypovolemia alone. During each of these conditions, superimposition of increased intra-abdominal pressure to 40 torr caused a further 26-43 per cent decrease in cardiac output compared with the pre-inflation value. Therefore, the greatest cardiovascular depression occurred when the animals were both hypovolemic and anesthetized with halothane. There was no difference in the responses to increased intra-abdominal pressure with the different inflating gases at any time. These findings indicate that in the presence of halothane anesthesia or hypovolemia, induction of pneumoperitoneum may cause severe cardiovascular depression.

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

To determine whether orally administered propranolol contributes to untoward hemodynamic function during general anesthesia, the authors divided patients undergoing myocardial revascularization into two groups: One group (n = 9) did not receive propranolol orally in the preoperative period. The other group (n = 10) received oral doses until five to six hours before induction of anesthesia, and the majority had demonstrable serum propranolol levels. Control (preanesthetic) hemodynamic values were determined following morphine—scopolamine premedication and percutaneous vascular cannulation. Post-intubation measurements were done following the sequence of thiopental, 2-3 mg/kg, succinylcholine, 1 mg/kg, and orotracheal intubation. Measurements were repeated at the following intervals after starting halothanenitrous oxide and pancuronium, 0.1 mg/kg: 5, 15, 30, and 60 min. Comparison of hemodynamic values in the propranolol and nonpropranolol groups revealed significantly lower heart rates at all measurement periods in the propranolol group. The groups showed no differences in cardiac output, mean arterial pressure, stroke volume, systemic peripheral vascular resistance, blood-gas, pH, or acid—base values. Patients in both groups responded to the “stress” of endotracheal intubation with increased heart rates and mean arterial pressures. In the absence of overt resting myocardial pain and frank left ventricular power failure, continuing oral administration of propranolol in moderate doses (average 140 mg/ day) until a few hours before general anesthesia with thiopental-succinylcholine-nitrous oxide- halothane and pancuronium does not appear to lead to unusual hemodynamic function in patients who have coronary-artery disease.

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

The effects of heparin, protamine, and the heparin-protamine complex on the abilities of platelets to aggregatein vitroin response to adenosine diphosphate (ADP) and epinephrine were determined. Citrated blood was obtained from normal volunteers and portions were treated with heparin, protamine, and three different ratios of heparin and protamine. The threshold concentrations of ADP and epinephrine required to produce complete platelet aggregation were then determined. Compared with control citrated plasma, the geometric mean of the threshold concentration for ADP in the heparinized sample was decreased twofold, from 1.88 to 0.94 μM; and that for epinephrine more than threefold, from 0.5 to 0.14 μM. In contrast, the threshold concentration for ADP was increased to 3.68 μM in the neutralized and to 2.78 μM in the overneutralized samples and that for epinephrine to 1.62 μM in the neutralized and 1.82 μM in the overneutralized samples. These data indicate that heparin increases the sensitivity of platelets to ADP and epinephrine as determined by platelet aggregation, and protamine added to heparinized blood not only reverses this effect, but decreases platelet sensitivity when it is added in concentrations that neutralize heparin. Additional protamine has no further effect, and protamine alone has no effect on platelet aggregation.

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1978

数据来源: OVID