Pagliaro P, Gattullo D, Linden R J, Losano G, Westerhssof N
Division of Biomedical Sciences, King's College London, London WC2R 2LS, UK.
Exp Physiol. 1998 Nov;83(6):821-31. doi: 10.1113/expphysiol.1998.sp004162.
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.
本研究旨在探讨左心室压力和心肌收缩状态对麻醉犬收缩期冠状动脉血流的影响。研究了包括生理范围在内的广泛左心室收缩压范围。实验在最大血管舒张和低灌注压力条件下进行,以避免血管自身调节干扰,并使微血管压力保持在正常范围内。在五只使用体外循环系统灌注的麻醉犬中,通过向心室内乳胶球囊注水,使心室容积以10 ml的步长从20 ml变化至50 ml,并测量左心室压力和冠状动脉血流的相关变化。然后将容积扩大至70 ml以产生过度拉伸,这会导致心脏收缩力短暂下降。在心脏收缩力较低的时期,将容积以10 ml的步长恢复至20 ml。收缩期心室压力随容积变化,但在收缩力较低的时期较低。对于收缩压低于100 mmHg的情况,压力与冠状动脉收缩期血流之间无显著关系,但在收缩力较低时,这种关系转变为较高的血流。对于收缩压高于100 mmHg的情况,收缩期冠状动脉血流在收缩压升高时显著下降。在这种情况下,收缩力降低前后关系的斜率无显著差异。这些发现表明,对于收缩压低于100 mmHg(即低于生理范围),收缩期心室的屏蔽作用可防止心室压力传递至心肌壁。当收缩压超过100 mmHg时,屏蔽作用被克服,收缩期血流减少的幅度随心室压力而变化。