{Reference Type}: Journal Article {Title}: Low dose alcohol exacerbates hyperdynamic circulation and shunting in non-alcoholic cirrhotic rats. {Author}: Pun CK;Huang HC;Chang CC;Hsu SJ;Chuang CL;Huang YH;Hou MC;Lee FY; {Journal}: Biosci Rep {Volume}: 0 {Issue}: 0 {Year}: 2024 Jul 5 {Factor}: 3.976 {DOI}: 10.1042/BSR20240354 {Abstract}: BACKGROUND: Portal hypertension affects hepatic, splanchnic and portosystemic collateral systems. Although alcohol is a well-known risk factor for liver cirrhosis, it also affects vascular contractility. However, the relevant effects on portal hypertension have not been evaluated in non-alcoholic cirrhosis. This study aimed to investigate the impacts of low-dose alcohol on portal hypertension-related derangements in non-alcoholic cirrhotic rats.  Methods: Sprague-Dawley rats received bile duct ligation to induce cirrhosis or sham operation as controls. The chronic or acute effects of low-dose alcohol (2.4 g/kg/day, oral gavage, approximately 1.3 drinks/day in humans) were evaluated.

 Results: The chronic administration of low-dose alcohol did not precipitate liver fibrosis in the sham or cirrhotic rats, however it significantly increased splanchnic blood inflow (P=0.034) and portosystemic collaterals (P=0.001). Mesenteric angiogenesis and pro-angiogenic proteins were upregulated in the alcohol-treated cirrhotic rats, and poorer collateral vasoresponsiveness to vasoconstrictors (P<0.001) was noted. Consistently, acute alcohol administration reduced splenorenal shunt resistance. Collateral vasoresponsiveness to vasoconstrictors also significantly decreased (P=0.003).

 Conclusions: In non-alcoholic cirrhosis rats, a single dose of alcohol adversely affected portosystemic collateral vessels due to vasodilatation. Long-term alcohol use precipitated splanchnic hyperdynamic circulation, in which mesenteric angiogenesis played a role. Further studies are warranted to evaluate the benefits of avoiding low-dose alcohol consumption in patients with non-alcoholic cirrhosis.