Hypothermia induced by inhibition of fatty acid metabolism in anesthetized rats: contributions of the forebrain and vagal afferents.

2-Mercaptoacetate (MA) is an antimetabolic drug that inhibits the utilization of fatty acids as an energy source. The intravenous injection of MA (1.2 mmol·kg-1) elicited an increase in tail skin temperature and a decrease in body core temperature in urethane-chloralose-anesthetized, neuromuscularly blocked, artificially ventilated rats, although administration of the same amount of NaCl did not. The respiratory exchange ratio was significantly higher after administration of MA than that after the saline treatment. On the other hand, heat production was increased by either the MA- or NaCl-injection, suggesting a nonspecific effect caused by the hyperosmolality of the solutions. These results indicate that the MA-induced hypothermia was caused by an increase in heat loss but not by a decrease in heat production. The amplitudes of heat loss responses to MA in rats fasted overnight were significantly smaller than those in fed ones, suggesting a mechanism for suppression of heat loss in the fasted state. Rats pretreated with vagotomy, capsaicin-induced desensitization of sensory nerve fibers or decerebration did not exhibit the MA-induced hypothermic responses. It is possible that the MA-induced heat loss and hypothermia were mediated by the vagal afferents and required the forebrain for the full expression of the responses.