Key result
Increases in coronary flow (6-25 ml/min) decreased the A-V delay solely as a result of reduced propagation time in the A-V node, suggesting a positive dromotropic effect mediated by shear stress.
Why the study?
Does increased coronary flow reduce auricular-ventricular delay in isolated guinea pig hearts?
Does increased coronary flow reduce auricular-ventricular delay in isolated guinea pig hearts?
In isolated guinea pig hearts, increased coronary flow directly enhances A-V nodal conduction, likely mediated by shear stress.
May enhance AV nodal conduction via shear stress in isolated hearts; leaves open relevance to intact physiology or clinical arrhythmias.
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.
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Rubio et al. (1995) studied this question. Increases in coronary flow was evaluated on Auricular-ventricular (A-V) transmission delay. Increases in coronary flow (6-25 ml/min) decreased the A-V delay solely as a result of reduced propagation time in the A-V node, suggesting a positive dromotropic effect mediated by shear stress.
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