ANALYSIS OF APROTININ ON THE MEAN ARTERIAL-PRESSURE, CAROTID-ARTERY BLOOD-FLOW, AND HINDLIMB VASCULAR-RESISTANCE IN THE LIVE RAT, AND PULMONARY VASCULAR-RESISTANCE IN THE ISOLATED-PERFUSED RAT LUNG

The effects of aprotinin on mean arterial pressure, carotid artery blood flow, pulmonary vascular resistance, and systemic vascular resistance have not been well documented. Therefore, the responses of aprotinin on the mean arterial pressure, carotid artery blood flow and the changes in pulmonary and hindlimb vascular resistances were investigated in the rat using ultrasonic flow probe analysis, and in two isolated vascular bed preparations. In studies on cardiac output using ultrasonic flow analysis, injections of aprotinin, in doses of 70-7000 KIU intravenously (iv), resulted in no changes in carotid artery ultrasonic flow, suggesting no changes in cardiac output. In isolated blood-perfused lung studies under conditions of controlled pulmonary blood flow, aprotinin, in doses of 7-7000 KTU intra-arterially (ia), caused no significant changes in pulmonary arterial perfusion pressure. Aprotinin, in doses of 7-240 KIU, was injected iv into the hindquarters perfusion circuit, and hindquarters arterial perfusion pressure did not change. Additionally, in the hindquarters perfusion preparation, aprotinin, in doses of 70-7000 KIU, ia resulted in no changes in mean arterial pressure. The present data demonstrate aprotinin has no significant response in MAP, carotid artery blood flow, pulmonary vascular resistance, or hindlimb vascular resistance in the rat.