Effects of contraction, perfusion pressure, and length on intramyocardial pressure in rat papillary muscle
Heslinga, J.W.; Allaart, C.P.; Yin, F.C.; Westerhof, N.
American Journal of Physiology 272(5 Pt 2): H2320-H2326
1997
ISSN/ISBN: 0002-9513 PMID: 9176301 Document Number: 483622
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 (P-zf). Therefore we determined P-zf and IMP at zero flow (IMP-zf) in papillary muscles suspended isometrically in a bath, superfused with a well-oxygenated Tyrode solution (27 degree 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 mu-M. During diastolic arrest and systolic contracture (2 mM Ba-2+), perfusion pressure steps were applied, and the corresponding flow and IMP values were recorded. Fitting of the relationships yielded P-zf and IMP-zf. In the diastolically arrested muscle, perfusion pressure affected IMP. P-zf was much higher in systolically contracted muscle than in diastolically arrested muscle. The IMP-zf in both conditions was significantly smaller than P-zf. 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.