Coronary flow stimulates auricular-ventricular transmission in the isolated perfused guinea pig heart.
In the heart in situ coronary flow stimulates oxygen consumption, glycolytic flux, myocardial contractility, and the release of bioactive substances. Studies have indicated that the coronary flow-enhanced contraction is similar to a hormonelike effect because the enhanced contraction results from an elevation in intracellular free calcium. In fact, if extracellular calcium is raised sufficiently, the contraction amplitude rises and remains constant and independent of coronary flow. We hypothesized that coronary flow could also stimulate other calcium-dependent cardiac functions such as auricular-ventricular (A-V) transmission. 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 propagation. When coronary vascular resistance was altered by dilation (nitroglycerin, bradykinin, nitroprusside, and adenosine) or by constriction (angiotensin II), this dromotropic effect of flow remained the same despite wide changes in perfusing pressure. Also, this dromotropic effect of flow was not altered by energy-altering substrates in the perfusate or by perfusion of adenosine receptor blockers. Furthermore, the effectiveness of flow as a dromotropic stimulus varied inversely with changes in calcium entry caused either by elevation or reduction of extracellular calcium. In addition, enhanced viscosity of the perfusing medium amplifies the positive dromotropic effect of flow. These results suggest that coronary flow is a stimulus that exerts a positive dromotropic effect mediated by shear stress.
D000628:Aminophylline / Q000494:pharmacology; D000818:Animals; D016275:Atrial Function; D002118:Calcium / Q000378:metabolism; D003326:Coronary Circulation / Q000502:physiology*; D004734:Energy Metabolism; D006168:Guinea Pigs; D006329:Heart Conduction System / Q000502:physiology*; D066298:In Vitro Techniques; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D009431:Neural Conduction / Q000502:physiology; D010477:Perfusion; D058915:Purinergic P1 Receptor Antagonists; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology; D016276:Ventricular Function; D014783:Viscosity
D007773:Lactates; D058915:Purinergic P1 Receptor Antagonists; D000628:Aminophylline; D019344:Lactic Acid; D002118:Calcium