Hemodynamic responses to different levels of alpha-adrenergic interruption in congestive heart failure.

The effects of prazosin, clonidine, and indoramin on central and regional hemodynamic parameters and left ventricular performance were analyzed in a congestive heart failure population to compare the pharmacodynamic responses to different levels of alpha-adrenergic interruption in this condition. The sympathetic nervous system is blocked at the peripheral alpha1-receptor by prazosin, at central nervous system alpha-receptor sites (via alpha-adrenoceptor agonism) by clonidine, and at peripheral and central sites by indoramin. Prazosin and indoramin produced reductions in total systemic and pulmonary vascular resistances, mean systemic and pulmonary artery pressures, and pulmonary capillary wedge pressure with little change in heart rate. Both agents selectively increased hepatic blood flow. Clonidine also decreased pulmonary artery pressure and vascular resistance, but evoked negative inotropic and chronotropic activity and did not alter regional blood flow. In contrast to prazosin, indoramin and clonidine did not augment cardiac output or stroke volume. In the setting of congestive heart failure, the central and regional hemodynamic effects and the responses in left ventricular performance vary considerably depending on the site of alpha-adrenergic interruption.