AJP - Heart and Circulatory Physiology, Vol 249, Issue 6 1070-H1077, Copyright © 1985 by American Physiological Society
Alpha 1-adrenergic blockade increases coronary blood flow during coronary hypoperfusion
I. Y. Liang and C. E. Jones
Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized
open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg.
Left coronary blood flow, as well as left ventricular oxygen extraction,
oxygen consumption, and contractile force were measured. The reduction in
perfusion pressure caused significant reductions in coronary flow, oxygen
consumption, and peak reactive hyperemic flow. During hypoperfusion in 11
dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist
prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22
and 16%, respectively. Peak increases were observed after 6-8 min of
prazosin infusion (0.6-0.8 mg prazosin), and both increases were
statistically significant (P less than 0.05). In seven additional dogs,
beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly
affect the actions of prazosin. In five additional dogs, the specific alpha
2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of
propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption
during coronary hypoperfusion. Those results suggest that an alpha 1- but
not an alpha 2-adrenergic constrictor tone was operative in the left
coronary circulation under the conditions of these experiments.
