摘要:

CommentIn the rat hypoxic model, fentanyl 100 μg/kg does not protect against cerebral high energy phosphate depletion or lactate accumulation when given prior to a 20-min hypoxic event.

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

CommentThis is a thorough and complete study that furthers our knowledge of the hepatic biochemical changes that occur prior to liver necrosis in guinea pigs exposed to halothane. Since the guinea pig appears to be the best animal model for evaluating the acute hepatotoxicity of halothane, and its response, in part, mimics the toxicity seen clinically, it is imperative that studies of this nature continue. That is, to find the mechanism by which halothane is selectively toxic to these animals (and by extrapolation toxic in humans). The researcher's emphasis on the delayed onset of lesion development in the guinea pigs is important. As they mention, the delayed onset affords the opportunity to study the chain of events that lead to the lesion formation. Past animal models not only did not mimic the toxicity seen clinically, but also produced either an immediate or mild transitory response. Once the chronology of cellular events from initiation (halothane exposure) to necrosis have been established, investigation can be undertaken to determine why halothane uniquely causes these events in guinea pigs and whether similar results can be expected in humans.The role of altered cell Ca++homeostasis in cell death is receiving considerable attention. This study demonstrates that halothane causes changes in hepatic and microsomal Ca++regulation similar to those observed with classic hepatotoxins (CCl4). However, since compounds like CCl4are hepatotoxic in a variety of species, how is it that halothane is specifically toxic in the guinea pig?One fault with the study is the absence of any comparative data following exposure to other volatile anesthetics (enflurane or isoflurane). Although these anesthetics have not been reported to cause alterations in serum enzymes or liver histology in guinea pigs, it is dangerous to assume that they may not affect biochemical or cellular processes. It will always be important to demonstrate that the alterations in liver homeostasis are unique to halothane and not the result of some generalized insult seen with any halocarbon.

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0039-6206    

出版商:OVID    

年代:1989

数据来源: OVID