AJP - Heart and Circulatory Physiology, Vol 253, Issue 6 1477-H1483, Copyright © 1987 by American Physiological Society
Prostacyclin reduces "preload" in conscious dogs via a vagal reflex mechanism
D. M. Nganele and T. H. Hintze
Department of Physiology, New York Medical College, Valhalla 10595.
The purpose of this study was to determine the effects of prostacyclin on
left ventricular (LV) preload in conscious dogs. LV end-diastolic diameter
(LV EDD) was used as an index of preload. Because prostacyclin reduces
arterial pressure, data were sampled when mean arterial pressure, heart
rate, and first derivative of LV pressure (dP/dt) had returned to control
levels. There was no dose-response relationship in the preload reduction to
prostacyclin, the threshold dose being 0.1 microgram/kg. Intravenous
prostacyclin (2.0 micrograms/kg) reduced LV EDD 2.9 +/- 0.5% from 36 +/-
2.2 mm, (P less than 0.01). With heart rate held constant (146 +/- 2.5
beats/min) by electrical pacing, prostacyclin still reduced LV EDD by 4.0
+/- 1.0% from 32 +/- 2.5 mm (P less than 0.05). Intravenous administration
of arachidonic acid (500 micrograms/kg) gave similar results. The magnitude
of the preload response to prostacyclin was similar to that of
nitroglycerin (25 micrograms/kg). Prazosin (1 mg/kg) or bilateral cervical
vagal section completely abolished the preload response to prostacyclin but
not to nitroglycerin. We, therefore, propose a mechanism where prostacyclin
activates cardiopulmonary receptors with vagal afferents that results in a
withdrawal of peripheral sympathetic tone to capacitance vessels to reduce
preload, in contrast to nitroglycerin, whose mechanism of action is most
probably a direct effect on capacitance vessels.
