Cardiorespiratory control by carotid chemoreceptors during experimental dives in the seal.

The diving responses of apnea and bradycardia, produced experimentally by immersing the face in water, were successfully elicited in the harbor seal Phoca vitulina anesthetized with urethan. The role of the carotid body chemoreceptors in the production of the diving bradycardia was studied in isolated carotid sinus-body preparations autoperfused with blood from the arterial circulation. When asphyxia was well developed during a dive the chemoreceptor drive was withdrawn by temporarily perfusing the chemoreceptors with blood of high PO2 (greater than 400 mmHg) and normal PCO2 from a disk oxygenator. The heart rate immediately rose to its predive value. Reestablishing hypoxic hypercapnic blood perfusion of the chemoreceptors from the animal's own circulation caused bradycardia with persistence of the apnea. Breathing restarted only on emersion. Substitution of normal arterialized blood from the oxygenator before or at the onset of a dive had no effect on the existing heart rate. It is concluded that the carotid bodies play an important part in maintaining the diving bradycardia during developing asphyxia without affecting respiration.