Abstract
In order to clarify the pathogenesis of hepatic coma, the effects of ammonia on pancreatic glucagon, insulin and blood glucose were studied in the patients with portal hypertension.
After an oral loading of ammonium chloride, plasma ammonia, glucagon, S-OCT and S-GOT increased remarkably in the patients with liver cirrhosis compared to those in the patients with hepatic fibrosis. In the cirrhotic patients, the basal concentration of glucagon were three times of that in the patients with hepatic fibrosis and the plasma glucagon increased as much as two times of the basal glucagon after 2 hours of an oral administration of ammonium chloride, while essentially unchanged in the patients with hepatic fibrosis. Glucagon concentration correlate closely to the degree of hyperammonemia in cirrhosis. However, insulin concentration and blood glucose were unchanged after an oral ammonia administration.
It is suggested that blood ammonia, elevated in cirrhosis, stimulates pancreatic glucagon secretion.
