Coronary flow stimulates auricular-ventricular transmission in the
isolated perfused guinea pig heart.
Rubio, Rafael, Guillermo Ceballos, and Jorge Suarez.
Department of physiology, University of Virginia, Charlottesville,
Va. 22908.
APStracts 2:0163H, 1995.
In the heart in situ coronary flow stimulate 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 hormone-like effect because the
enhanced contraction results from an elevation in intracellular free
calcium. In fact, if extracellular calcium is raised sufficiently the
contraction amplitude raises and remains constant and independent of
coronary flow. We hypothesized that coronary flow could also
stimulate other Ca++ dependent cardiac functions such as auricular
-ventricular transmission. This hypothesis was tested in isolated
guinea pig hearts perfused at constant flow. Our results show that
increases in coronary flow (6 to 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 (nitroglycerine, 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, nor
by perfusion of adenosine receptor blockers. Furthermore, the
effectiveness of flow as a dromotropic stimulus varied inversely with
changes in Ca++ entry caused either by elevation or reduction of
extracellular Ca++. In addition enhanced viscosity of the perfusing
media 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.
Received 16 May 1994; accepted in final form 10 April 1995.
APS Manuscript Number H416-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.