Experimental Physiology (1998), 83, 821-831 Printed in Great Britain SYSTOLIC CORONARY FLOW IMPEDIMENT IN THE DOG: ROLE OF VENTRICULAR PRESSURE AND CONTRACTILITY PASQUALE PAGLIARO*, DONATELLA GATTULLO, RONALD J. LINDENt, GIANNI LOSANO AND NICO WESTERHOFt Dipartimento di Scienze Cliniche e Biologiche dell'Universita di Torino, 10043 Orbassano, Italy, *Division of Biomedical Sciences, King's College London, London WC2R 2LS, UK and 4Laboratory for Physiology, Institute for Cardiovascular Research, ICaR-VU, Free University, Amsterdam, The Netherlands (MANUSCRIPT RECEIVED 1 APRIL 1998, ACCEPTED 19 AUGUST 1998) SUMMARY The present study was planned to investigate the effect of left ventricular pressure and inotropic state on coronary arterial inflow in systole in the anaesthetized dog. A wide range of left ventricular systolic pressures, including the physiological range, were studied. Experiments were done under conditions of maximal vasodilatation and low perfusion pressure in order to avoid vascular autoregulative interference and to keep the microvascular pressure within the normal range. In five anaesthetized dogs, perfused with extracorporeal circulation system, ventricular volume was changed from 20 to 50 ml in steps of 10 ml by filling an intraventricular latex balloon, and the related changes in left ventricular pressure and coronary flow were measured. The volume was then extended to 70 ml to obtain an overstretch which induced a transient decrease in cardiac contractility. During the period of low cardiac contractility the volume was brought back to 20 ml in steps of 10 ml. Systolic ventricular pressure changed with volume but was lower during the period of low contractility. For systolic pressures below 100 mmHg there was no significant relationship between pressure and coronary systolic flow, but the relationship shifted to higher flows during low contractility. For systolic pressures above 100 mmHg systolic coronary flow decreased significantly when systolic pressure increased. In this case the slopes of the relationships were not significantly different before and after the reduction in contractility. These findings suggest that for systolic pressures less than 100 mmHg (i.e. below the physiological range) the shielding effect of the contracting ventricle prevents the ventricular pressure from being transmitted in the myocardial wall. When systolic pressure exceeds 100 mmHg the shielding effect is overcome and the amplitude of the systolic flow reduction varies with ventricular pressure. INTRODUCTION It is well known that during the systolic phase the coronary arterial inflow is reduced (e.g. Klocke, 1976; Feigl, 1983). However, there is not yet full agreement about the mechanisms responsible for this reduction. The vascular waterfall model (Downey & Kirk, 1975) and the intramyocardial pump model (Spaan, Breuls & Laird, 1981) assume an extravascular (or intramyocardial) pressure which is proportional to left ventricular pressure (LVP) with a proportionality factor changing from unity at the endocardial side to zero at the epicardial side of the heart wall. The intra- myocardial pressure, which increases with ventricular pressure during contraction, decreases vascular transmural pressure and thus decreases coronary vascular volume and increases resistance. * Corresponding author: pagliaro@medfarm.unito.it 754 ) by guest on September 29, 2011 ep.physoc.org Downloaded from Exp Physiol (