[Perfusion and metabolism of liver and splanchnic nerve area under sevoflurane anesthesia]

Abstract

In common with other halogenated volatile anaesthetics, sevoflurane causes a dose-related cardiovascular depression and therefore the affection of blood flow of different organ systems is suggested. So far known, sevoflurane is not different compared to isoflurane in affecting liver and splanchnic blood flow. Concluded from former published studies there was no case of hepatic toxicity of sevoflurane been published so that this substance can be used in patients with reduced hepatic function. The primary organic metabolite of sevoflurane is hexafluorisopropanol (HFIP), which is readily and rapidly conjugated with glucuronic acid. No reactive intermediates are formed and HFIP appears to be an unlikely compound to form liver protein adducts. For this reasons sevoflurane "hepatitis" is not expected. Like most other inhalation agents sevoflurane increase the neuromuscular blockade after treatment with muscle relaxants in anaesthesia. The MAC values of Sevoflurane where reduced after the application of nitrous oxide, benzodiazepines and opiates. From human studies we know that chronic drug therapy with isoniazid induces the metabolism of sevoflurane, enflurane and isoflurane, markedly increasing peak plasma fluoride concentrations. However, barbiturates as well as phenytoin do not influence the metabolism of sevoflurane because these agents do not induce the major hepatic defluorinating enzyme cytochrome P450 2E1. Obesity, untreated diabetes mellitus and alcohol abuse increase the hepatic content and activity of cytochrome P450 2E1 and therefore enhanced anaesthetic defluorination is to be suspected. Until now, there are no studies about sevoflurane anaesthesia in patients after liver transplantation but the extremely low hepatotoxic potential as compared to isoflurane provides no argument to avoid this substance for anesthesia in liver transplanted patients.