The hemodynamic responses to terbutalinea selective p,-adrenoceptor agonistwere studied in conscious normal rats and in conscious rats with secondary biliary cirrhosis. Compared with those of normal rats, dose-response curves in cirrhotic rats indicated significantly decreased reactivity in arterial pressure and heart rate. Half-maximal effective dose was not significantly different between the two groups. Terbutaline induced significant, dose-dependent decreases in portal pressure in both normal rats (9.3%) and cirrhotic rats (13.8%). In normal rats, terbutaline administration (32 pg * min-* kg-l bodywt) increased both cardiac output and portal tributary blood flow, thus mimicking hemodynamic changes in cirrhotic rats. In cirrhotic rats, despite a significant increase in portal tributary blood flow (from 19.9 f 1.7 mllmin to 22.7 & 1.5 ml/min), terbutaline decreased portal pressure from 17.4 k 1.0 mm Hg to 15.0 2 0.8 mm Hg.
This study indicates that increased p,-adrenoceptor stimulation in cirrhotic rats may be involved in hyperdynamic circulation. The association of a decreased portal pressure and increased splanchnic blood flow suggests that p,-adrenoceptor stimulation may modulate hepatic and portal collateral vascular resistance. (HEPATOLOGY 1992;15:459-463.) p-adrenergic antagonists reduce the risk of gastrointestinal bleeding in patients with cirrhosis (1-3). This beneficial effect depends at least in part on reduction of portal pressure and reduction of blood flow into the superior portal systemic circulation (4). The mechanisms of action of P-blockers on the splanchnic circulation have not been, however, entirely elucidated. Nonselective p-blockers, however, are known to induce more profound splanchnic effects than cardioselective p-blockers (5). Thus it is thought that nonselective