Induction of lipid droplet accumulation in cardiac muscle cells of guinea pigs and mice: an analysis of the effects of reserpine and fasting.

Abstract

AbstractReserpine has been demonstrated in previous studies to induce the accumulation of lipid droplets in ventricular cardiac muscle cells of bats and this effect has been attributed to mediation by the sympathetic nervous system. The present study was done to evaluate the species specificity of this action of the drug. Reserpine caused lipid droplet accumulation in cardiocytes of guinea pigs and mice. However, in contrast to the action of the drug in bats, this action of reserpine in guinea pigs and mice could not be antagonized by chemical sympathectomy with 6‐hydroxydopamine or by treatment of animals with phenoxybenzamine, atropine or hexamethonium. Like reserpine, fasting for as little as 24 hours induced lipid droplet accumulation in cardiocytes of guinea pigs and mice. This effect also could not be prevented by treatment with 6‐hydroxydopamine indicating that the sympathetic nervous system was not involved in its mediation. Force‐feeding guinea pigs given reserpine prevented the accumulation of lipid droplets normally induced by this drug. It is concluded that the lipid droplets accumulation in the hearts of guinea pigs that follows administration of reserpine is not due to a direct cardiotoxicity of the drug but is secondary to the failure of drug‐treated animals to eat. Since the autonomic nervous system appears to mediate reserpine's cardiotoxicity in bats, the species difference revealed by these experiments probably results from an underlying physiological difference in the nervous systems of these animals.