Contractility is the main determinant of coronary systolic flow impediment.
We measured the relation between coronary flow amplitude (delta F = Fd-Fs; where d is diastolic and s is systolic) and developed left ventricular pressure (delta PLV = Ps-Pd) at a constant perfusion pressure of 75 mmHg (10 kPa) in the maximally vasodilated blood-perfused isolated cat heart for different steady-state levels of contractility (protocol A) and during transients in contractility (protocol B). Contractility was defined as the slope of the end-systolic pressure-volume relation (Emax). From protocol A it appeared that the coronary flow amplitude was only weakly related to left ventricular pressure at each steady-state level of contractility studied. However, the coronary flow amplitude was strongly related to the different levels of contractility. In protocol B, contractility was changed over a wide range of values (0-100%) but developed pressure and contractility changed simultaneously. Using multiple linear regression analysis, we found that contractility has approximately 10 times (range: 2.8-57.3) stronger effect than left ventricular pressure on coronary flow amplitude (n = 10 experiments). These data and our earlier observations suggest that it is the difference in stiffness of cardiac muscle between systole and diastole that determines coronary flow amplitude.
Krams
R
R
Laboratory for Physiology, Free University of Amsterdam, The Netherlands.
Sipkema
P
P
Zegers
J
J
Westerhof
N
N
D000818:Animals; D001794:Blood Pressure; D002415:Cats; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000502:physiology*; D005263:Femoral Artery / Q000502:physiology; D006339:Heart Rate; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction; D010477:Perfusion; D011312:Pressure; D013997:Time Factors; D016276:Ventricular Function