In a canine model, volume load-induced tachycardia is regulated by both sympathetic and vagal efferentation, whereas bradycardic responses are primarily driven by changes in sympathetic efferentation.
Should not alter clinical volume management; leaves open differential autonomic control of tachycardia versus bradycardia in humans.
The influence of 42 i.v. infusions of saline on heart rate, sympathetic and vagal cardiac efferent activity and on the aortic baroreceptor and left atrial B-type nerve impulse activity was studied in 32 morphine-chloralose anesthetized dogs. The responses in heart rate were tachycardic in 31 infusions and bradycardic in 11 infusions. In tachycardia, sympathetic activity increased in a majority of the cases but also decreases and nonsignificant changes were observed. Vagal efferentation decreased in most of the cases but also nonsignificant changes or increases in activity occurred. Sympathetic efferentation mainly decreased in bradycardic responses while vagal efferentation diverged in different directions in its nerve activity rate. The ratio of sympathetic to vagal impulses significantly correlated to the heart rate in most of the cases in tachycardia but not in bradycardia. It is concluded that sympathetic and vagal cardiac efferentation plays a significant role in heart rate regulation in volume load-induced tachycardia but in bradycardia only the changes in sympathetic cardiac efferentation are important in respect to heart rate changes. The aortic baroreceptor and left atrial B-type receptor activity rate increased both in tachycardia and bradycardia. Changes in the activities of these receptors do not explain the different heart rate responses. It is supposed that bradycardic responses result from changes in cardiac contraction associated with some reflex mechanism suppressing the excitatory influence of the activity of atrial receptors on sympathetic cardiac efferentation.
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M. O. K. Hakumäki (1979) studied this question.
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