Kingma J G, Martin J, Rouleau J R
Quebec Heart Institute, Sainte Foy, Canada.
Am J Physiol. 1994 Jul;267(1 Pt 2):H133-8. doi: 10.1152/ajpheart.1994.267.1.H133.
Instantaneous diastolic left coronary artery pressure-flow relations (PFR) shift during acute tamponade as pressure surrounding the heart increases. Coronary pressure at zero flow (Pf = 0) on the linear portion of the PFR is the weighted mean of the different myocardial waterfall pressures, the distribution of which varies across the left ventricular wall during diastole. However, instantaneous PFR measured in large epicardial coronary arteries cannot be used to estimate Pf = 0 in the different myocardial tissue layers. During coronary vasodilatation in a capacitance-free model, myocardial PFR differs from subendocardium to subepicardium. Therefore, we studied the effects of acute tamponade during maximal pharmacology induced coronary vasodilatation on myocardial PFR in in situ anesthetized dogs. Tamponade reduced cardiac output, aortic pressure, and coronary blood flow. Results demonstrate that different mechanisms influence distribution of myocardial blood flow during tamponade. Subepicardial vascular resistance is unchanged and the extrapolated Pf = 0 is increased, thereby shifting PFR to a higher intercept on the pressure axis. Subendocardial vascular resistance is increased while the extrapolated Pf = 0 remains unchanged. Results indicate that in the setting of acute tamponade with coronary vasodilatation different mechanisms regulate the distribution of myocardial blood flow: in the subepicardium only outflow pressure increases, whereas in the subendocardium only vascular resistance increases.
急性心包填塞时,随着心脏周围压力升高,左冠状动脉瞬时舒张压-血流关系(PFR)发生改变。在PFR的线性部分,零流量时的冠状动脉压力(Pf = 0)是不同心肌瀑布压的加权平均值,在舒张期其分布在左心室壁上有所不同。然而,在大的心外膜冠状动脉中测量的瞬时PFR不能用于估计不同心肌组织层的Pf = 0。在无容量模型中冠状动脉血管扩张期间,心肌PFR从心内膜下到心外膜下有所不同。因此,我们研究了在最大药理学诱导的冠状动脉血管扩张期间急性心包填塞对原位麻醉犬心肌PFR的影响。心包填塞降低了心输出量、主动脉压力和冠状动脉血流量。结果表明,心包填塞期间不同机制影响心肌血流分布。心外膜下血管阻力不变,外推的Pf = 0增加,从而使PFR在压力轴上的截距升高。心内膜下血管阻力增加,而外推的Pf = 0保持不变。结果表明,在冠状动脉血管扩张的急性心包填塞情况下,不同机制调节心肌血流分布:在心外膜下仅流出压力增加,而在心内膜下仅血管阻力增加。