title: Coronary arterial inflow impediment during systole is little affected by capacitive effects.
abstract: During cardiac contraction coronary arterial inflow is impeded, whereas venous flow is augmented. These effects are assumed to be caused by diameter reductions of intramyocardial blood vessels. The reduction in vascular diameter (and thus vascular volume) during contraction increases coronary resistance and/or decreases back pressure so that flow decreases and the rate of change of volume results in a capacitive flow. The aim of this study was to estimate the contribution of capacitive flow to total coronary inflow impediment. Isolated blood-perfused (100 mmHg and constant), maximally vasodilated, ryanodine-pretreated rat hearts (n = 8) with intraventricular balloons were used. The coronary inflow impediment during isovolumic beats at a heart rate of 2-3 Hz (dynamic contractions) and during prolonged systoles obtained by fast pacing (static contractions, no capacitive flow impediment) were compared. Changing left ventricular balloon volume enabled us to vary left ventricular pressure and to relate systolic flow to systolic left ventricular pressure. We found that for the same contractility (expressed in terms of systolic pressure-volume relationship and maximal elastance) and same left ventricular pressure, the ratio of coronary inflow impediment in dynamic and static contractions is not significantly different from unity (P < 0.005). This implies that under our experimental conditions coronary inflow impediment in dynamic contractions is little affected by capacitive effects.
authors.affiliation: Laboratory for Physiology, Institute for Cardiovascular Research, Free University, Amsterdam, The Netherlands.
authors.forename: P
authors.initials: P
authors.lastname: Bouma
authors.forename: P
authors.initials: P
authors.lastname: Sipkema
authors.forename: N
authors.initials: N
authors.lastname: Westerhof
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D003331:Coronary Vessels / Q000033:anatomy & histology / Q000502:physiology*; D004837:Epinephrine / Q000494:pharmacology; D006339:Heart Rate; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D011312:Pressure; D051381:Rats; D011921:Rats, Inbred WKY; D012433:Ryanodine / Q000494:pharmacology; D013599:Systole / Q000502:physiology*; D014664:Vasodilation; D016277:Ventricular Function, Left
chemical_list: D012433:Ryanodine; D004837:Epinephrine