Published online Aug 28, 2005. doi: 10.3748/wjg.v11.i32.5025
Revised: December 18, 2004
Accepted: December 21, 2004
Published online: August 28, 2005
AIM: To investigat the relation between hepatotoxicity of halothane and sevoflurane and altered hepatic calcium homeostasis in enzyme-induced hypoxic rats.
METHODS: Forty-eight rats were pretreated with phen-obarbital and randomly divided into six groups (eight in each group) and exposed to O2/ N2/1.2 MAC anesthetics for 1 h: normal control (NC), 21% O2/79% N2; hypoxic control (HC), 14% O2/86%N2; normal sevoflurane (NS), 21% O2/ N2/1.2MAC sevoflurane; hypoxic sevoflurane (HS), 14% O2/ N2/1.2MAC sevoflurane; normal halothane (NH)21%O2/79%N2/1.2MAC halothane; hypoxic halothane (HH), 14% O2/N2/1.2MAC halothane. Liver specimens and blood were taken 24 h after exposure to calcium and determined by EDX microanalysis.
RESULTS: The liver of all rats given halothane (14% O2) had extensive centrilobular necrosis and denaturation. Morphologic damage was accompanied with an increase in serum glutamic pyruvic transminase. In groups NH and HH, more calcium was precipitated in cytoplasm and mitochondria.
CONCLUSION: These results suggest that halothane increases cytosolic Ca2+ concentration in hepatocytes. Elevation in Ca2+ concentration is implicated in the mechanism of halothane-induced hepatotoxicity. sevoflurane is less effective in affecting hepatic calcium homeostasis than halothane.