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AJP - Heart and Circulatory Physiology, Vol 272, Issue 5 2320-H2326, Copyright © 1997 by American Physiological Society
ARTICLES |
J. W. Heslinga, C. P. Allaart, F. C. Yin and N. Westerhof
Laboratory for Physiology, Vrije Universiteit, Amsterdam, The Netherlands.
If intramyocardial pressure (IMP) is the pressure that causes coronary flow to stop, i.e., "backpressure," then it should be equal to the zero-flow perfusion pressure intercept (Pzf). Therefore we determined Pzf and IMP at zero flow (IMPzf) in papillary muscles suspended isometrically in a bath, superfused with a well-oxygenated Tyrode solution (27 degrees C), and perfused with Tyrode solution via the septal artery. For the IMP (servo-null) measurements, we used unbeveled glass micropipettes with a tip diameter of 3-4 microns. During diastolic arrest and systolic contracture (2 mM Ba21), perfusion pressure steps were applied, and the corresponding flow and IMP values were recorded. Fitting of the relationships, yielded Pzf and IMPzf. In the diastolically arrested muscle, perfusion pressure affected IMP. Pzf was much higher in systolically contracted muscle than in diastolically arrested muscle. The IMPzf in both conditions was significantly smaller than Pzf. Thus, even in this preparation with no ventricular pressure, IMP increases during contraction. We conclude that IMP arises from contraction per se but is not the pressure that causes the flow to stop.
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