Neural, hormonal and intrinsic mechanisms of cardiac control during acute coronary occlusion in the intact dog.

Three basic mechanisms may be involved in the control of cardiac function during acute coronary occlusion: (1) neural; (2) hormonal (circulating catecholamine); and (3) intrinsic (e.g. Frank--Starling law). The response of intact, sedated (Innovar-Vet, 0.08 cc/kg), chronically instrumented dogs to a 5 min left circumflex coronary occlusion was tested to delineate the relative roles of each of the above mechanisms. First, 6 innervated and 6 cardiac denervated dogs were examined. The major difference between groups was that the occlusion-induced tachycardia was significantly smaller in the denervated dogs than in the normally innervated animals (+10 +/- 7 vs +27 +/- 4/min, respectively, (mean +/- S.D.)). Changes in the first time derivative of left ventricular pressure (d(LVP)/dt) were similar (--898 +/- 556 vs --796 +/- 274 mm Hg/sec, denervated vs innervated). Decreases in stroke volume and mean arterial pressure were also similar in the two groups. The occlusion-induced tachycardia was compared in a second group of denervated dogs (n = 5) before and after administration of propranolol to examine the role of circulating catecholamines, and, by exclusion, to observe the response of the heart per se, independently of extrinsic control factors. The heart rate response was similar in both cases (+8 +/- 4 vs +6 +/- 4/min, unblocked vs blocked). Finally, blood pressure was prevented from falling during coronary occlusion in 3 normally innervated dogs by coupling the femoral artery to a reservoir of saline suspended above the animals. Blunting the input to the baroreceptors in this manner did not significantly change the size of the occlusion-induced tachycardia. We conclude that during acute coronary occlusion in dog: (1) the major role of the cardiac nerves involves modulating changes in the chronotropic state of the heart; (2) changes in d(LVP)/dt result principally from intrinsic phenomena linked to ischemia-induced alterations in myocardial performance; (3) changes in circulating catecholamines play only a minor role in controlling the heart during acute coronary occlusion in denervated dog; and (4) receptors located within the heart figure significantly in the etiology of the occlusion-induced tachycardia.