摘要:

The purpose of the present study was to determine the effect of intravenously administered epinephrine on the maternal cardiovascular response and uterine artery blood flow velocity (UBFV) in the pregnant guinea pig. Epinephrine (0.2, 0.5, and 1.0 µg/kg) and lidocaine (0.4 mg/kg, with and without 0.2 µg/kg of epinephrine) were administered intravenously to seven chronically instrumented pregnant guinea pigs near term. Lidocaine without epinephrine did not significantly alter maternal heart rate (MHR), maternal mean arterial pressure (MMAP), or UBFV. Epinephrine, with and without lidocaine, resulted in a transient decrease in MHR. Further, epinephrine, with and without lidocaine, resulted in significant elevations in MMAP and significant, dose-related reductions in UBFV. Mean (±SEM) UBFV was 72 ± 4%, 56 ± 4%, and 40 ± 5% of baseline at 30 s after administration of epinephrine, 0.2, 0.5, and 1.0 µg/kg, respectively. It is concluded that these small intravenous boluses of epinephrine result in significant, although transient, reductions in UBFV in the pregnant guinea pig.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The authors determined the effects of aminophylline on the anesthetic requirements for halothane in rats and dogs. MAC for halothane was determined in rats (n=24) before and after aminophylline, 100 mg · kg−1ip, or an equal volume of saline. Because changes in central noradrenergic neurotransmission have been linked to drug-induced changes in the depth of the anesthetic state, we investigated the effect of aminophylline on the turnover of norepinephrine in discrete brain regions of halothane-anesthetized rats. To facilitate testing at steady-state aminophylline conditions and to permit frequent blood sampling, halothane MAC was determined in dogs (n=7) before and after a therapeutic level of aminophylline (15 ± 2 µg · ml−1) was obtained. Neither in the rats (1.0 vs. 1.0%) nor in the dogs (1.04 ± 0.14 vs. 1.01 ± 0.14%) was halothane MAC affected by aminophylline treatment. Commensurate with the lack of change of anesthetic depth, aminophylline treatment did not affect noradrenergic neurotransmission in the brain of halothane-anesthetized rats. Furthermore, the anticipated increase in circulating catecholamines following aminophylline treatment in dogs did not materialize. The authors conclude that halothane anesthetic requirements are not altered by aminophylline treatment, possibly because of the attenuation of the putative sympathomimetic effects of aminophylline by halothane.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

In earlier work on malignant hyperthermia (MH) susceptible pigs the concentration of muscle metabolites differed from that found in normal control pigs. Therefore, in the present study these metabolites were measured in human muscle biopsies to find out whether normal individuals could be discriminated from MH-susceptible persons. Analysis of skeletal muscle metabolites was performed on skeletal muscle obtained from humans (n = 68) being screened to exclude or confirm susceptibility to MH. Three groups were identified based on the reaction pattern of a skeletal muscle sample exposed in vitro to caffeine or halothane 1% plus caffeine: 1) MH susceptible (MHS; n — 19); 2) normal humans, (controls; n = 31); and 3) intermediatereaction type (K-type: n = 18). No significant differences were found in metabolite levels of phospbocreatine (normal, MHS, and K-type: 13.20 vs. 13.74 vs. 14.42 nmol/mg wet weight, respectively), creatine (16.30vs. 16.94vs. 15.06 nmol/mg wet weight, respectively), adenosine triphospate (3.75 vs. 3.98 vs. 3.89 nmol/mg wet weight, respectively) and lactate (3.73 vs. 3.65vs. 3.79 nmol/mg wet weight, respectively). It is concluded that analysis of skeletal muscle metabolites cannot be used as a screening test to confirm or exclude MH susceptibility in humans.

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1986

数据来源: OVID