Perfusion induced changes in oxygen consumption and cardiac
contractility (gregg effect) are mediated through different
mechanisms.
Dijkman, Marieke A., Johannes W. Heslinga, Pieter Sipkema, Nico
Westerhof.
Laboratory for Physiology, Institute for Cardiovascular Research.
ICaR-VU, Vrije Universiteit Amsterdam, The Netherlands
APStracts 3:0111H, 1996.
Increased cardiac perfusion results in increased oxygen consumption
and increased contractility (Gregg phenomenon) in the isolated heart.
We investigated if these two aspects of the Gregg phenomenon are
related to coronary flow or arterial pressure. Coronary flow and
(thus) arterial pressure (Part) were changed in the reference state
and during vasoconstriction (3 nM Vasopressin) in the Langendorff
perfused rat heart contracting isovolumically (ventricular balloon)
at 27 degrees C (n=5). All hearts showed an increase in developed
isovolumic left ventricular pressure (dev Plv, measure of
contractility) and in oxygen consumption (VO2) with increased
perfusion. Developed Plv depended primarily on Part so its relation
with coronary flow was shifted by vasoconstriction. Conversely, VO2
was primarily depended on coronary flow so its relationship with Part
was shifted with vasoconstriction. Using vasoconstriction (decreased
vascular radii) the effects of arterial pressure and wall shear
stress (proportional to Part x radius) should be separable but the
results did not reach significance. Thus contractility is related to
arterial pressure or shear stress while oxygen consumption is related
to coronary flow. We conclude that the two aspects of the Gregg
phenomenon are based on different mechanisms.
Received 13 November 1995; accepted in final form 8 March 1996.
APS Manuscript Number H1065-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96