Carotid chemoreceptor reflex parasympathetic coronary vasodilation in the dog.

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.