[Ventricular volume and coronary flow].

Abstract

This study aimed at investigating the role of ventricular volume (VV), left ventricular pressure (LVP) and myocardial contractility in causing changes in coronary flow (CF), in the absence of autoregulation. Changes in VV and, consequently, in LVP and myocardial contractility were induced in 5 anesthetized dogs using an extracorporeal circulation including a heart-lung machine. Left VV was changed in steps of 10 ml, from a lowest value of 10 ml to a maximum value of 70 ml and back, by introducing and subtracting different volumes of water in and from a latex balloon placed in the left ventricle. In order to suppress any interference by autoregulatory mechanisms, the experimental manoeuvres were performed in the presence of complete coronary vasodilation obtained with dipyridamole. Each increase in VV was accompanied by an increase in diastolic LVP which was in turn responsible for a greater development of pressure by the myocardial contraction, thus producing an increase in systolic LVP. Then, the pressure developed by the myocardial contraction, considered as the difference between systolic and diastolic LVP, decreased when the ventricle was dilated to 60 and 70 ml. Diastolic CF decreased only starting from a ventricular volume of 60 ml, varying independently of the changes in diastolic LVP. In addition, the amplitude of the coronary flow reduction in systole was found to change together with the pressure developed by the myocardial contraction with which showed a significant linear correlation. During the reduction in VV, a progressive fall of diastolic LVP occurred without any significant difference with respect to the phase of increased volumes; on the contrary, systolic LVP, at each ventricular volume, was lower than in the previous phase. Also diastolic CF, when the volume was progressively reduced, was lower than in the previous manoeuvre. The amplitude of the systolic flow reduction and the pressure produced by the contraction both decreased when the ventricular volume was reduced showing a significant linear correlation. The reduction of the pressure produced by the contraction is likely to be due to a loss of contractility after the ventricle was expanded more than 3 times its resting volume. It is concluded that changes in ventricular pressure do not influence phasic CF directly and that diastolic CF decreases only following extreme ventricular dilation. Finally, systolic flow reduction is seen to depend on the myocardial contractility and not on the levels reached by the pressure inside the ventricle.