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How does the denervated transplanted heart respond to physiologic and pharmacologic stimuli?
How does the denervated transplanted heart respond to physiologic and pharmacologic stimuli?
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The transplanted, denervated heart increases cardiac output during exercise primarily through increased stroke volume, with delayed heart rate increases likely mediated by both circulating catecholamines and intrinsic cardiac mechanisms.
Hemodynamic observations were performed one and six months after cardiac transplantation in a 46-year-old man. Cardiac catheterization revealed normal pressures at rest and a slightly decreased cardiac index. Total cardiac denervation was documented by absence of reflex changes in heart rate during physiologic and pharmacologic stimuli. Intracardiac electrocardiography demonstrated both donor and recipient p waves, the former always controlling the heart rate. Observations during atrioventricular dissociation indicated that the transplanted heart has active atrial transport. The denervated heart responded to the stress of muscular exercise. Cardiac output increased predominantly by increasing stroke volume, although delayed increments in heart rate occurred. After complete beta-adrenergic blockade, the response of the heart rate to exercise was attenuated but not completely blocked. These findings suggest that whereas circulating catecholamines have an important role in cardiac acceleration during exercise, an additional mechanism, intrinsic to the heart itself, may be responsible for the increase in heart rate.
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Shaver et al. (1969) studied this question.
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