Coronary flow stimulates @entity67 transmission in the isolated perfused XXXX heart.

@entity859 @entity1242 @entity26 @entity840 @entity1854 @entity2224 @entity460 @entity1812 @entity67
In the heart in situ coronary flow stimulates @entity26 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 @entity460 . In fact, if extracellular @entity460 is raised sufficiently, the contraction amplitude rises and remains constant and independent of coronary flow. We hypothesized that coronary flow could also stimulate other @entity460 -dependent cardiac functions such as @entity67 ( @entity67 ) transmission. This hypothesis was tested in isolated @entity840 hearts perfused at constant flow. Our results show that increases in coronary flow (6-25 ml/min range) decrease the @entity67 delay solely as a result of reduced propagation time in the @entity67 node and not in @entity2224 . When coronary vascular resistance was altered by dilation ( @entity1242 , @entity1812 , @entity1854 , and @entity859 ) 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 @entity859 receptor blockers. Furthermore, the effectiveness of flow as a dromotropic stimulus varied inversely with changes in @entity460 entry caused either by elevation or reduction of extracellular @entity460 . 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.
