CORONARY FLOW STIMULATES AURICULAR-VENTRICULAR TRANSMISSION IN THE ISOLATED-PERFUSED GUINEA-PIG HEART

In the heart in situ coronary flow stimulates oxygen consumption, glyc olytic flux, myocardial contractility, and the release of bioactive su bstances. Studies have indicated that the coronary flow-enhanced contr action is similar to a hormonelike effect because the enhanced contrac tion results from an elevation in intracellular free calcium. In fact, if extracellular calcium is raised sufficiently, the contraction ampl itude rises and remains constant and independent of coronary flow. We hypothesized that coronary flow could also stimulate other calcium-dep endent cardiac functions such as auricular-ventricular (A-V) transmiss ion. This hypothesis was tested in isolated guinea pig hearts perfused at constant flow. Our results show that increases in coronary flow (6 -25 ml/min range) decrease the A-V delay solely as a result of reduced propagation time in the A-V node and not in atrial or ventricular pro pagation. When coronary vascular resistance was altered by dilation (n itroglycerin, bradykinin, nitroprusside, and adenosine) or by constric tion (angiotensin II), this dromotropic effect of flow remained the sa me despite wide changes in perfusing pressure. Also, this dromotropic effect of flow was not altered by energy-altering substrates in the pe rfusate or by perfusion of adenosine receptor blockers. Furthermore, t he effectiveness of flow as a dromotropic stimulus varied inversely wi th changes in calcium entry caused either by elevation or reduction of extracellular calcium. In addition, enhanced viscosity of the perfusi ng medium amplifies the positive dromotropic effect of flow.