Effects of Prostaglandin A1 on the Systemic and Coronary Circulations in the Conscious Dog
The effects of intravenous prostaglandin A1 (PGA1) on systemic and coronary hemodynamics were studied in 13 intact, conscious dogs after recovery from operation for implantation of Doppler ultrasonic flow probes on the ascending aorta and left circumflex coronary artery. Graded doses of PGA1 (0.01 to 1.0 µg/kg) caused arterial pressure and total systemic resistance to decrease progressively and heart rate and cardiac output to increase progressively. At the maximum dose administered (1.0 µg/kg), arterial pressure and systemic resistance decreased by averages of 30% and 51% below control, respectively, and heart rate and cardiac output rose 64% and 47%, respectively. After beta-receptor blockade with propranolol, PGA1 still caused a similar increase in cardiac output. In spite of arterial hypotension, PGA1 produced a progressive increase in coronary flow, with a peak increase of 74% above control with 1.0 µg/kg and a corresponding graded decrease in coronary resistance, with a decrease of 61% below control with 1.0 µg/kg. Marked increases occurred in systolic as well as diastolic coronary flow. The coronary vasodilation was not abolished by preventing the PGA1-induced tachycardia with electrical pacing, by beta-receptor blockade, or by combined blockade of beta receptors and cholinergic nerve fibers. While arterial Po2 remained constant, coronary sinus Po2 rose when coronary flow was increased by PGA1. Thus PGA1 is both a primary and secondary coronary vasodilator which increases cardiac output and decreases total systemic resistance.
- Received November 30, 1970.
- Accepted March 24, 1971.
- © 1971 American Heart Association, Inc.