Effect of length and contraction on coronary perfusion in isolated perfused papillary muscle of rat heart.

We studied the impeding effect of cardiac muscle contraction on coronary arterial inflow in six isolated, perfused papillary muscles 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 s or by doubling the calcium concentration in the perfusate and the superfusion fluid from 1 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-1.g-1 during diastole to 12.4 +/- 1.8 (SE) ml.min-1.g-1 at peak systole, P < 0.001] 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-1.g-1, P < 0.05), and systolic flow decreased by 3% (12.4 +/- 2.3 to 12.0 +/- 1.6 ml.min-1.g-1, P = NS). 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 ml.min-1.g-1, 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.