Treatment of hepatic coma and hepatorenal syndrome: Mechanism of action of L-dopa and aramine

Abstract

An attempt is made to unify the pathophysiology of the cerebral, cardiovascular, and renal complications of hepatic failure by postulating the accumulation of false neurochemical transmitters in the presynaptic storage sites of the peripheral and central adrenergic nervous system. Such an hypothesis is consistent with many widely accepted clinical and biochemical observations previously made about hepatic failure, hepatic coma, and the hepatorenal syndrome. It may explain the recently described beneficial effects of L-dopa on the mental and circulatory status of patients in hepatic failure and the occasionally successful treatment of the hepatorenal syndrome with large doses of metaraminol or other alpha-adrenergic amines. Experimental findings obtained in both laboratory animals and patients are presented.