ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The protective effect of barbiturates in cerebral ischemia has been proposed to be related to inhibition of lipid peroxidation. The presentin-vitrostudy was undertaken to test the efficiencies of different barbiturates to inhibit peroxidative reactions in brain tissue, and to compare their effects with established free radical scavengers (chlorpromazine and promethazine). Cortical homogenates, prepared from decapitated rats, were incubated at 37 C with 5 per cent O2(in N2) in the presence of ferrous sulfate (0.01 mM) and ascorbic acid (0.25 mM). During incubation there was extensive lipid peroxidation in the tissue, as evidenced by appreciable production of thiobarbituric acid-reactive material (TBAR), 1.2 μmol malondialdehyde g−1cortex in one hour. Thiopental (1.0 mM) caused a 96 per cent inhibition of TBAR production, while other barbiturates (in the same concentrations) had only small (methohexital) or no (pentobarbital and phenobarbital) inhibitory effect. The inhibition of TBAR production by 1.0 mM thiopental was similar to that found with 1.0 mM chlorpromazine or 0.1 mM promethazine. The inhibitory effect of thiopental on lipid peroxidation was confirmed by analysis of fatty acids and phospholipids. Thiopental prevented the peroxidative degradation of polyenoic (20:4, 22:6) fatty acids and of ethanolamine phosphoglyceride that otherwise occurred during incubation.The marked differences between the tested barbiturates with respect to their abilities to inhibit lipid peroxidationin vitroare at variance with the fact that all of these barbiturates have been reported to protect the ischemic brain in various situationsin vivo.The results imply that the protective effect of barbiturates under such conditions is unrelated to inhibition of lipid peroxidation, and suggest that instead they may act by other mechanisms.

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Mutagenic activity of urines obtained from operating room personnel was assayed in the AmesSalmonella/mammalian microsome system using three strains of histidine-dependentS. typhimurium, TA1535, TA1538, and TA100. Two procedures were employed. In the first, 100− and 200-μl aliquots of urine obtained from 28 subjects working in either scavenged or unscavenged operating rooms were tested. In the second, urine samples obtained from 13 physicians before and after starting an anesthesia residency, as well as 250-fold concentrates of these samples, were assayed. There was no statistically significant difference in urinary mutagenic activities between individuals working in scavenged and those working in unscavenged operating rooms. Furthermore, urines of anesthesiologists collected before and after beginning training had similar mutagenic activities. Only heavy smokers had mutagenic urine. It was concluded that the majority of operating room workers do not excrete mutagens in the urine.

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Ryanodine toxicity in animals has been suggested to constitute a model of malignant hyperthermia. Dantrolene is known to block the development of malignant hyperthermia triggered by halothane in susceptible swine. The authors studied the influences of dantrolene and halothane on the effects of ryanodinein vitroin isolated rat diaphragm muscle segments, andin vivoin mice, to explore the validity of this model. In the diaphragm experiments, dantrolene was found to block or delay the development of contractures produced by ryanodine and to delay the potentiation of ryanodine-induced contractures caused by halothane. In mice, ryanodine at various dosages was injected and animals surviving after one hour were examined. Such survivors appeared grossly to be normal, and may constitute a model for the malignant hyperthermia patient. They were found to be susceptible to halothane and to succinylcholine, being killed by treatment with these two agents at dosages that were not lethal to control mice. Pretreatment of mice for 48 hours with orally administered dantrolene, followed by injection of ryanodine and then halothane anesthesia, decreased the lethality of ryanodine but did not reduce the number of deaths caused by the subsequent exposure to halothane. That the effects of ryanodinein vitroandin vivoare diminished and potentiated by dantrolene and halothane, respectively, would suggest that the ryanodine toxicity model of malignant hyperthermia may have validity and is worthy of further study. A prediction from this model is that the terminal cisternae of skeletal muscle sarcoplasmic reticulum may be altered in MH.

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

To assess the effects of chronic exposure to low levels of nitrous oxide on neural function of man, the authors evaluated the neurologic condition, motor and sensory nerve conduction, and computerized tests of sensation of approximately half of the dentists in Rochester, Minnesota. Results of scored tests of neural function were not significantly different for dentists who used nitrous oxide extensively in their practices and dentists who did not. To assess the effects of chronic exposure to high levels of nitrous oxide on neural function and structure of experimental animals, groups of rats were exposed to 70 per cent N2O in 30 per cent oxygen for four hours, five days a week, for six months. Rats exposed to N2O and control rats showed no difference in well-being, in caudal nerve conduction, in axonal content and transport of acetylcholinesterase and dopamine-β-hydroxylase, or in number and size distribution and pathologic abnormality of teased myelinated fibers. Although these results indicate a lack of peripheral nerve neurotoxicity of N2O in the rat, one cannot assume a similar lack of neurotoxicity in man with heavy exposures.

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The effects of hypotension (40–50 torr range) as induced by inhalation of halothane (2–3 per cent), halothane (0.75 per cent) plus sodium nitroprusside (0.2–0.4 mg/kg/min), or halothane (0.75 per cent) plus trimethaphan (4–16 mg/kg/min) on total and regional cerebral blood flow (tCBF, rCBF) in the goat were measured by radioactive microsphere distribution technique. Inhalation of halothane (2–3 per cent) alone caused an average reduction in tCBF of 25 per cent, with no significant reduction in regional flow except in cortical white matter, which showed a 42 per cent reduction. Halothane with sodium nitroprusside infusion caused an average 45 per cent decrease in tCBF and significant decreases in blood flows to the thalamus (42 per cent), cerebellum (41 per cent), cortical gray matter (35 per cent), and white matter (58 per cent). Halothane with trimethaphan infusion produced a reduction in tCBF (47 per cent), associated with significant decreases in blood flows to the thalamus (36 per cent), cerebellum (41 per cent), cortical gray matter (22 per cent), and white matter (47 per cent). Both halothane with sodium nitroprusside and halothane with trimethaphan produced significantly greater reductions of blood flows to the thalamus, cerebellum, and gray and white matter than did 2–3 per cent halothane. In addition, both caused significantly greater reductions in tCBF than did 2–3 per cent halothane. Of all the brain regions studied, only the hypophysis showed no statistically significant reduction in rCBF no matter which technique was used to produce hypotension. Conversely, cortical white matter appeared to be the region most affected by each technique.

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Cerebral vascular and metabolic effects of lorazepam were evaluated in ten awake monkeys by use of a modification of the Kety-Schmidt technique. Five received ketamine, 10 mg/kg, im, five to eight hours prior to the study, but all animals were otherwise treated identically. Monkeys receiving ketamine had significantly greater (P< 0.05) cerebral blood flow (CBF) values before lorazepam was given (46 ± 1 ml/100 g/min) than did monkeys not receiving ketamine (41 ± 1 ml/100 g/min), but in all other respects, premedicated and unpremedicated animals did not differ. Lorazepam administration did not significantly alter systemic arterial blood pressure or blood-gas values. However, it did decrease CBF by 26 per cent and increase cerebral vascular resistance (CVR) by approximately 25 per cent (P< 0.01). The cerebral metabolic rate for glucose (CMRμ) decreased 42 per cent (P< 0.05). Following lorazepam administration, the cerebral metabolic rate for oxygen (CMRO2) decreased by 21–30 per cent. When combined CMRO2data for the two anesthetic groups are pooled, this decrease is significant (P< 0.05). This study indicates that sedative doses of lorazepam decrease cerebral blood flow and metabolism with minimal effects on blood pressure and blood-gas values. Lorazepam administration did not produce any change in cerebral metabolism indicative of brain hypoxia or ischemia.

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Previous studies have shown that halothane inhibits glucose-stimulated insulin secretion. This study was designed to determine whether the mechanism of inhibition involves a reduction in glucose metabolism. The effects of halothane on glucose (16.7 mM)-stimulated insulin secretion and glucose oxidation were studied in isolated rat pancreatic islets. Halothane, 0.11 mM (0.5 MAC), 0.22 mM (1.0 MAC), and 0.33 mM (1.5 MAC), inhibited glucose-stimulated insulin release in a dose-related manner by 5.2 per cent (NS), 21.0 per cent (P< 0.05), and 32.6 per cent (P< 0.01), respectively. At the 0.33 mM (1.5 MAC) concentration, halothane did not significantly inhibit the oxidation of 6-14C-glucose to14CO2, although higher concentrations of halothane did result in significant inhibition. The data suggest that halothane's inhibitory effect on glucose-stimulated insulin secretion is not due to interference with glucose oxidation.

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1980

数据来源: OVID