Electrocardiogram of the diving seal.

THE DIVING mechanism in the seal is believed to be comprised of two major changes in the circulation which afford an efficient means of maintaining an adequate oxygen supply to the brain for a prolonged period of inability to breathe. One circulatory response to diving is the arterial constrictor response which prevents the flow of blood through muscle beds during the dive. Therefore, the muscle mass does not remove oxygen from the circulating blood, and a high blood oxygen saturation is maintained for a longer period of time. Accompanying this decrease in perfused vascular bed is the other circulatory alteration, bradycardia with decrease in cardiac output.' 3 This bradycardia appears to be reflex in origin, inasmuch as it may begin within one heart beat of submersion, and it is so consistent that an electrocardiogram may be used to clock the periods of diving. This type of reflex bradycardia with diving was first reported by Bert in 1870, when he found that the duck developed bradycardia when its head was submerged in water. Since that time, the diving-reflex bradycardia has been reported in the penguin, beaver, muskrat, porpoise, seal, rabbit. Florida manatee, and water snakes. In 1899. Richet demonstrated that the administration of atropine to the duck would prevent the duck from being able to dive. Irving et al. reported that atropine prevented the reflex bradycardia in the porpoise. Porster and Xyboer found that the atropinized rabbit did not have reflex brady-