R. Rubio et al., CORONARY FLOW STIMULATES AURICULAR-VENTRICULAR TRANSMISSION IN THE ISOLATED-PERFUSED GUINEA-PIG HEART, American journal of physiology. Heart and circulatory physiology, 38(4), 1995, pp. 1177-1185
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.