Systemic and splanchnic hemodynamic effects of molsidomine in rats with carbon tetrachloride–induced cirrhosis

Molsidomine, a long‐acting vasodilator mainly used as an antianginal agent, was reported to decrease the portohepatic venous pressure gradient in patients with alcoholic cirrhosis. This study investigated the effects of linsidomine, the active metabolite of molsidomine, on systemic and splanchnic hemodynamics in rats with CCI4‐induced cirrhosis using the microsphere technique. Compared with placebo‐treated rats, linsidomine‐treated animals were found to have a significant decrease in portal venous pressure (– 18%, p < 0.01) and in mean arterial pressure (–16%, p < 0.01), smaller peripheral resistances (p < 0.01), greater portal venous inflow (p < 0.05), smaller splanchnic arteriolar resistances (p < 0.01) and smaller portocollateral resistances (p < 0.05). Cardiac output, hepatic arterial blood flow, portal blood flow and estimated hepatic blood flow were not significantly different between the two groups of animals. Linsidomine‐treated rats exhibited a trend toward greater collateral blood flow compared with controls, but this difference was not significant. We conclude that linsidomine decreases portal venous pressure by reducing portocollateral resistances without affecting liver blood flow. These effects should be beneficial for patients with cirrhosis and portal hypertension. (HEPATOLOGY 1991;13:1181–1184.)