Effect of length changes and contraction on coronary perfusion in
isolated perfused papillary muscle of rat heart.
Allaart, Cornelis P., and Nico Westerhof.
Laboratory for Physiology, Institute for Cardiovascular Research,
ICaR-VU
APStracts 3:0058H, 1996.
We studied the impeding effect of cardiac muscle contraction on
coronary arterial inflow in six isolated perfused papillary muscle of
the rat. Special attention was given to the effect of changes in
muscle length and contractility on flow impediment in systole.
Contractility was changed by resumption of pacing after a quiescent
period of 60-100 seconds or by doubling the calcium concentration in
the perfusate and the superfusion fluid from 1 mM to 2 mM. The
vascular bed was maximally dilated with adenosine and perfusion
pressure was kept constant at 69 +/- 3 cmH2O. We found that
contractions impede arterial inflow by 29% (from 17.3 +/- 2.2
ml/min/g during diastole to 12.4 +/- 1.8 ml/min/g at peak systole,
p<0.001, mean +/- SEM) while the muscle was kept at 90% of
maximum muscle length (MLmax). When the muscle was stretched from 80%
to 97% of MLmax, diastolic force increased from 0.5 +/- 0.3 to 11.1
+/- 1.2 mN/mm2, systolic force increased from 11.1 +/- 1.5 to 44.6
+/- 4.0 mN/mm2, diastolic flow decreased by 12% (from 18.2 +/- 2.3 to
15.9 +/- 1.9 ml/min/g, p<0.05) and systolic flow decreased by 3%
(12.4 +/- 2.3 to 12.0 +/- 1.6, n.s.). Increased contractility by
elevated [Ca2+] did not affect diastolic flow but increased systolic
flow impediment from 29% to 39% (systolic flow decreased from 12.4
+/- 1.8 to 10.3 +/- 1.4, p<0.01). The results are qualitatively
similar to findings in the intact heart. Limitations on quantitative
comparison due to differences in muscle architecture and differences
in force vectors in the papillary muscle and the left ventricle are
discussed. The results show that ventricular pressure is not
essential in systolic coronary arterial flow impediment. The findings
are in agreement with the varying elastance concept where the flow
impediment is predicted to depend on myocardial elastic properties.
Received 24 April 1995; accepted in final form 24 January 1996.
APS Manuscript Number H384-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96