AJP - Heart and Circulatory Physiology, Vol 249, Issue 6 1167-H1175, Copyright © 1985 by American Physiological Society
Carotid chemoreceptor reflex parasympathetic coronary vasodilation in the dog
B. R. Ito and E. O. Feigl
The hypothesis that carotid body chemoreceptor activation with
hypoxic-hypercapnic blood elicits reflex coronary vasodilation was
investigated. Circumflex or anterior descending coronary artery blood flow
was measured in alpha-chloralose-anesthetized, closed-chest dogs. To
minimize changes in cardiac metabolism, the heart was paced at a constant
rate after atrioventricular heart block, propranolol (1 mg/kg) was given to
prevent beta-receptor-mediated alterations in cardiac contractility, and
aortic blood pressure was stabilized by means of a blood reservoir. The
carotid body regions were vascularly isolated and perfused at constant
pressure with arterial blood or hypoxic-hypercapnic blood. Under these
conditions, carotid body chemoreceptor stimulation with hypoxic or
hypoxic-hypercapnic blood for 90 s produced atrial bradycardia and a
transient increase in coronary blood flow of 36-53% above prestimulation
values. The augmented coronary flow was accompanied by a transient increase
in coronary sinus O2 tension of 4.6-5.7 mmHg. Aortic blood pressure varied
less than 10 mmHg. Intracarotid injections of nicotine (0.1 microgram/kg)
or cyanide (150 micrograms) produced similar results. The coronary response
to chemoreceptor stimulation with hypoxic blood or drugs was abolished when
the reflex arc was interrupted with atropine (0.5 mg/kg). It is concluded
that transient reflex parasympathetic coronary vasodilation is elicited by
hypoxic or hypoxic-hypercapnic stimulation of carotid body chemoreceptors.
