Footshock stress accelerates carbon tetrachloride-induced liver injury in rats: Implication of the sympathetic nervous system

Abstract

The effects of electric footshock stress on carbon tetrachloride (CCl4)-induced liver injury were examined in rats. Plasma glutamate-pyruvate transminase (GPT) activity was used as an index of acute liver injury and liver collagen content as chronic injury. When rats were given 6-h footshock starting 6 h after CCl4 injection, the plasma GPT activity was remarkably increased 24 h and 48 h after CCl4 injection, although either CCl4, or footshock alone had no significant effect on plasma GPT acivity. Upon repetition of the CCl4 plus footshock treatments to rats once a week for 10 weeks, proliferation of liver collagen was more pronounced than upon CCl4 injections alone, which was demonstrated histologically as well as biochemically. Pretreatment of rats with reserpine or 6-hydroxydopamine caused a marked suppression of the increase in plasma GPT activity after CCl4 plus footshock treatments. Surgical hepatic denervation also tended to suppress and hepatic denervation plus adrenodemedullation completely suppressed the increase of plasma GPT activity after CCl4 plus footshock treatments. The results suggest that footshock stress can potentiate CCl4-induced liver injury mainly through activation of both hepatic sympathetic innervation and the adrenal medulla.