1982 Volume 23 Issue 10 Pages 1158-1165
Gastrointestinal bleeding is a common complication in patients with liver cirrhosis and the main sources of hemorrhage are ruptured esophageal or gastric varices and acute gastric erosions. However, the mechanism leading to the onset of hemorrhage remains unclear, although some authors emphasize the importance of increased portal venous pressure in initiating a bleeding episode. We examined incidents related to the onset of hemorrhage in patients with liver cirrhosis, and we detected some patients with bleeding after alcohol intake. Then, we examined the effects of ethanol, its metabolite, acetaldehyde and catecholamine (epinephrine) released from the adrenal medulla and the adrenergic nerve terminals by ethanol and acetaldehyde on portal circulation, by means of the isolated perfused liver in the normal and cirrhosis rat. We clarified that ethanol itself have no effect on portal circulation. Acetaldehyde increased an intrahepatic portal vascular resistance in the normal liver, but not in the cirrhotic liver. Epinephrine increased markedly an intrahepatic portal vascular resistance in the normal and cirrhotic liver. Thus, it is possible that alcohol ingestion leads to the rupture of esophageal or gastric varices.
