Why the study?
Does increased afterload induce the release of myocardial catecholamines to regulate cardiac output in the intact dog heart?
Does increased afterload induce the release of myocardial catecholamines to regulate cardiac output in the intact dog heart?
Increased afterload triggers the release of myocardial catecholamines, which contributes to the regulation of cardiac output in the intact dog heart, whereas catecholamine-depleted hearts rely solely on the Frank-Starling mechanism.
Indicates adrenergic mediation of afterload responses in intact hearts; leaves open relevance to human cardiac disease.
K jekshus , J. and O. D. M jøs . Effect of increased afterload on the inotropic state and uptake of free fatty acids in the intact dog heart. Acta physiol. scand. 1972. 84. 415–427. In anesthetized dogs treated with atropine and pentolinium tartrate–a ganglionic blocking agent–the possibility was tested that release of myocardial catecholamines contributes to the regulation of cardiac output during increased outflow resistance. When left ventricular systolic pressure was raised by an average of 100 mm Hg (from 99 to 193 mm Hg), cardiac output increased (+34 %) from 122 to 163 ml/min kg and maximum rate of rise of left ventricular pressure (dP/dt) (+ 50%) from 1.30 to 1.80 mm Hg 10 ‐3 /s. Myocardial uptake of free fatty acids (FFA) showed an average increase of 221 % (from 2.9 to 9.3 μEq/min 100 g), in spite of unchanged arterial FFA concentrations, indicating adrenergic activation of the heart. These responses were abolished following a similar rise in left ventricular systolic pressure (from 88 to 184 mm Hg) in reserpine‐treated dogs during ganglionic blockade. Changes in left ventricular end‐diastolic pressure, as well as myocardial oxygen consumption, were similar in both groups. The present study supports the conclusion that catecholamines are released from myocardial stores during augmented intraventricular pressure, thereby explaining the increase in cardiac output. However, in the catecholamine‐depleted heart, cardiac output is maintained by the Frank‐Starling mechanism alone.
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Kjekshus et al. (1972) studied this question.
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