摘要:

&NA;Methionine synthetase (MS) activity in the brain and liver is decreased following nitrous oxide (N2O) exposure. Since MS is important for DNA synthesis, this interaction would be expected to have the most serious consequences on actively replicating tissue. The authors therefore measured MS activity in rat testes following 1 h exposure to either 10% or 50% N2O. Animals exposed to 10% N2O had a 29% reduction in MS activity, and exposure to 50% N2O caused a 63% reduction in enzyme activity. Testicular MS activity returned to normal by 24‐48 h in the 10% exposure group and by 72 h in the 50% exposure group. This biochemical effect on testicular enzyme activity could be the basis for the reported deleterious effects of N2O on spermatogenesis.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

&NA;The influence of inhalational anesthetics on histamine released during bronchospasm induced by Ascaris antigen aerosol was studied in Basenji‐Greyhound (BG) dogs. Five BG dogs were anesthetized with thiopental and halothane on separate occasions and challenged with Ascaris antigen aerosol for five minutes. Pulmonary resistance (RL), dynamic compliance (Cdyn). and arterial plasma histamine levels were measured over 30 min following antigen exposure.Prior to antigen challenge, RL, Cdyn, and histamine levels were similar in thiopental‐ and halothane‐anesthetized dogs. The peak change in RL, and Cdynoccurred 10 min after the start of antigen challenge. RL, increased 3.0 ± 0.4‐fold (mean ± SEM) in thiopental‐anesthetized dogs as compared with 1.6 ± 0.2‐fold in halothaneanesthetized dogs (P < 0.05). Cdyndecreased to a similar extent in both groups, with maximal decreases of 0.53 ± 0.08 and 0.53 ± 0.09 times the prechallenge value for thiopental‐ and halothane‐anesthetized dogs, respectively. Plasma histamine levels peaked at 5 min. Plasma histamine increased to 8.0 ± 5.0 ng/ml in thiopental‐anesthetized dogs compared with 10.7 ± 4.7 ng/ml in halothane‐anesthetized dogs. Histamine levels were not significantly different during or after antigen challenge between thiopental‐ and halothane‐anesthetized dogs.Halothane, but not thiopental, significantly attenuated the increase in RLprovoked by antigen challenge. However, arterial plasma histamine levels were similar during both anesthetics. Therefore, the authors conclude that the protective effect of halothane on airways was not due to an inhibition of release of histamine from mast cells.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

&NA;Although fentanyl has been used widely as a short‐acting narcotic analgesic, its metabolism in humans has not been clarified. In this study, three fentanyl metabolites were identified in the urine of eight surgical patients receiving 0.3‐0.5 mg of fentanyl intravenously. The metabolites 4‐N‐(N‐propionylanilino)piperidine, 4‐N‐(N‐hydroxypropionylanilino)piperidine and l‐(2‐phenethyl)‐4‐N‐(N‐hydroxypropionylanilino)piperidine, and unchanged fentanyl were identified by GC‐mass spectrometry in urine collected 6 h after administration. Fentanyl and its main metabolite, 4‐N‐(N‐propio‐nylanilino)piperidine, were determined quantitatively in the urine of five additional patients receiving 0.5 mg fentanyl intravenously. Urinary excretion of fentanyl and 4‐N‐(N‐propionylanilino)‐piperidine during the first 12 h after injection accounted for 0.3‐4.0% and 26 to 55% of the dose, respectively.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

&NA;The effects of halothane on uptake and phosphorylation of uridine, and on cellular ATP content were studied inTetrahymena pyriformis,a ciliate protozoan. Exposure to halothane inhibited the accumulation of14C‐uridine into the following acid‐soluble intracellular pools: UTP, UDP, UMP, and an unidentified compound. Halothane did not alter ATP content of intact cells. It is concluded that inhibition by halothane of uridine incorporation into RNA ofT. pyriformisis due to effects on uridine uptake and/or phosphorylation and not due to inhibition of the RNA polymerase reaction or reduction of ATP content.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID