APStracts 3:0544H, 1996.

Effects of contraction, perfusion pressure, and length on intramyocardial pressure in rat papillary muscle.. Heslinga, J. W., C. P. Allaart, F. C. P. Yin, and N. Westerhof. Laboratory for Physiology, Institute for Cardiovascular Research (ICaR-VU), Vrije Universiteit, van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands, Cardiology Division, Johns Hopkins Hospital, Baltimore MD 21205

APStracts 3:0544H, 1996.

If intramyocardial pressure (IMP) is the pressure that causes coronary flow to stop, i.e., "back" pressure, 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's solution (27 degrees C), and perfused with Tyrode's solution via the septal artery. For the IMP (servo-null) measurements we used unbevelled glass micropipettes with a tip diameter of 3 to 4 [mu]m. During both diastolic arrest and systolic contracture (barium, 2 mM), 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 as compared to diastolically arrested muscle. The IMPzf in both conditions was significantly smaller than Pzf. Thus, even in this preparation with no ventricular pressure, IMP rises during contraction. We conclude that IMP arises from contraction per se but is not the pressure that causes the flow to stop.

Received 7 June 1996; accepted in final form 4 December 1996.
APS Manuscript Number H506-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996