ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Excretion of methoxyflurane was studied in 12 patients receiving anesthesia in a closed rebreathing circuit at a constant alveolar concentration of approximately 0.24 per cent. The mean methoxyflurane uptake was 1S g (range 7.6–31 g) during a mean time of anesthesia administration of 2 hours. 1S minutes (range 55–309 minutes). An average of 19 per cent of the uptake was recovered unchanged in the exhaled air after anesthesia. Urinary excretion of organic fluorine, fluoride, and oxalic acid was equivalent to 29, 7.7 and 7.1 per cent of methoxyflurane uptake. respectively. Approximately a third of the uptake remained unrecovered. It is postulated that a portion of the unrecovered drug became permanently bourn to tissues and hence its exeretion was delayed beyond the period of the study.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

The kinetics of biotransformation of methoxyflurane by rat hepatic microsomesin vitrowas studied. The rate or biotransformation as measured by analysis of metabolites continued to increase even at near-saturation concentrations of the anesthetic. Methoxyflurane biotransformation followed either an unbounded curve with empirical formula y = a ln(bx + I) or an asymptotic curve with formula y = x/ax+b No substrate inhibition was observed, Total fluoride Vmaxof 135.1 mμmol F-/mg protein/30‘ was increased to 931.9 by phenobarbital induction: free fluoride Vmaxfrom 39.2 to 403.2. Thus, enzyme induction shifted biotransformation to the production of greater amounts of inorganic free fluoride metabolites than organic fluoride-contaning metabolites, Phenobarbital induction caused qualitative as well as quantitative alteration in the biotransformation of methoxyflurane.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Killing of tumor cells by lymphoid cells is important in cell-mediated immunity and defense against cancer. The authors determined that halothane, invitro, inhibits the killing of YAAC-1 ascites tumor cells from A/jax mice by sensitized peritoneal exudate cells from C57/Black/6 mice. Lysis of tumor cells was quantitated by release of51Cr into the culture medium. Inhibition of cell-mediated cytotoxicity ranged from 3 per cent in 0.5 per cent halothane to 44.7 per cent in 2.5 per cent halothane and was related to the duration of halothane exposure. A 12 per cent inhibition of cytotoxicity by 80 per cent nitrous oxide was not statistically significant, but was of a magnitude near that of an equipotent concentration of halothane. The inhibition of cytotoxicity by halothane and nitrous oxide observedin vitromay partially account for the inhibition of cytotoxicity observed when patients undergo surgical operation.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

in vitrotests of cell-mediated immunity were performed using blood obtained from subjects with unexplained hepatitis following halothane anesthesia to determine whether sensitization to potentially antigenic products of halothane metabolism might exist. Both lymphocyte transformation and leukocyte migration-inhibition tests were undertaken in the presence of trifluoroacetylated human liver specific protein and trifluoroacetylated human serum albumin. All tests in the presence of these potential antigenic complexes were negative. The results support the view that cell-mediated hypersensitivity to trifluoroacetylated proteins does not contribute to the pathogenesis of hepatic dysfunction following halothane anesthesia

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Using a specific and sensitive radioimmunoassay, naloxone concentrations in the brains and sera of rats were measured at intervals for four hours following iv injection (5 mg/kg). Decrement curves of naloxone were compared with those after iv injection of morphine (5 mg/kg). Serum concentration of naloxone at 5 minutes was 1.45 ± 0.1 μg/ml (mean ± SE) and that of morphine was 1.0 ± 0.08 μg/ml. Their serum half-lives from one to four hours were approximately the same. 30–40 minutes. With naloxone. the brain-serum concentration ratios ranged from 2.7 to 4.6. Concentration of naloxone in the brain declined parallel to that in the serum. However, with morphine the initial brain concentration was approximately one tenth that in the serum (0.096 ± 0.04 μg/ml). The brain morphine concentration was sustained for one hour. while serum morphine concentrations declined from 1.0 to 0.19 μg/ml during this period. Two minutes after iv injection of naloxone HCl (0.4 mg) in nine healthy volunteers, the serum drug concentration was 0.01 ± .001 μg/ml. At 5 minutes. 97 per cent of the administered dose was no longer found in the serum, the serum concentration being 0.004 ± .0003 μg/ml. From 20 minutes to two hours after injection, the calculated mean serum half-life of naloxone was 64 minutes. These results suggest that the rapid penetrance of naloxone into the brain and the high brain-serum concentration ratio contribute to its rapid onset of action and potency as a narcotic antagonist. The rapid decline of naloxone concentration in the brain found in the animal model, in contrast to that of morphine, could be the basis for its relatively short duration of action.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Chronically catheterized dogs were studied awake and during anesthesia with high and low concentrations of halothane to assess the relationship between cardiac function and metabolism. Low concentrations of halothane (0.79 per cent endtidal) increased heart rate and decreased left ventricular stroke volume, stroke work, and dP/dt without producing other hemodynamic changes. However, similar heart rate increases produced by atrial pacing in awake animalsincreasedaortic pressure and cardiac output anddecreasedleft atrial pressure. Consequently, the halothane-induced tachycardia partially compensated for the negative inotropic effect of the halothane. High concentrations of halothane (1.74 per cent endtidal) Further increased heart rate and elevated left atrial pressures. Cardiac output, stroke volume, stroke work, aortic pressure. LV dP/dt, myocardial blood flow and oxygen consumption were markedly decreased. Myocardial glucose extraction was also decreased. Myocardial oxygen extraction was unchanged, and lactate extraction rose with both concentrations of halothane. Consequently, the dose-dependent negative inotropic effect of halothane resulted in a decrease in cardiac oxygen demand which was equal to or greater than the decrease in oxygen delivery. Whether the same relationship would be seen in the ischemic heart is yet to be demonstrated

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

The losses of righting reflex produced by various doses of phenobarbetal in mice at 1 atm O2versus 1 atm O2plus 102 atm He were determined. The resulting dose-response curve at pressure gave an ED50that was 64 per cent larger than the ED50at 1 atm. This increment is essentially the same as that found for gaseous anesthetics under similar test conditions. The quantitative similarity of the results of pressure reversals of barbiturate and inhalational anesthetics suggests that the mechanisms or sites of action of these agents are similar. However, the dose-response curve at 103 atm was steeper than that at 1 atm. This raises an alternative possibility that anesthetics and pressure bear no mechanistic relationship to each other, but rather that pressure produces a generalized central nervous system stimulation that would antagonize any depressant effect.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID