A hypoxic rat model of halothane-induced hepatotoxicity, which is known to
produce liver damage, was used to determine the effects of chronic exercise
on halothane-induced hepatotoxicity and on reduced hepatic glutathione (GS
H) levels. Metabolism of volatile anesthetics may generate metabolites that
can cause mild and transient hepatotoxicity. Methods: Six male Sprague-Daw
ley rats completed a IO-wk (5 d.wk(-1)) treadmill running protocol. Twelve
age-matched animals were used as sedentary controls. After the completion o
f exercise training, rats were exposed for 2 h to 1% halothane in 14% O-2.
Twenty-four hours later, animals were anesthetized with sodium pentobarbita
l and sacrificed. Livers were excised, stained, and evaluated for hepatotox
icity using a histopathological 0 (normal) to 5 (severe damage) point categ
orical scale and for the determination of GSH levels. Results: Median histo
pathologic scores revealed significantly lower indications of hepatotoxicit
y in exercise animals as compared with control animals (score = 0.25 vs 1.5
0; P < 0.05). Liver damages scores between 1 and 5 were observed in 75% (9
of 12) of the control animals, whereas only 1 of 6 exercise animals had a s
core greater than 1 (P < 0.05). No significant difference was observed in r
educed GSH levels. Conclusions: Chronic exercise improves the detoxicant ab
ility of the liver for halothane anesthesia as noted by the ameliorated liv
er damage and reduced incidence of halothane-induced hepatotoxicity in the
exercise animals.