CORONARY CAPACITANCE AND VENTRICULAR DYSFUNCTION

心肌是高度血管化的，心肌内冠状血管是 能够储存冠状动脉血流。 此前，小 冠状静脉系统和冠状流出道一直受到关注 压力 然而，如果心肌内血容量或电容 它主要位于冠状静脉、小静脉和毛细血管中， 冠状动脉流出（静脉）压可能是主要的 心肌充盈和左室舒张压的决定因素 扩张性，因为流出压力的变化应该有效地 通过低静脉阻力传递到微循环。 我们 总体目标是评估冠状静脉压的作用， 心肌内血液储存：（a）作为LV舒张压的决定因素 功能，和;（B）在冠状动脉血流的调节。 实验 将在具有LV的离体血液灌注犬心脏中进行 等容收缩。 我们将评估冠状静脉 压力对左室舒张期压力-容积关系的影响 协议. 在方案I中，右心房和心室（RV）压力将 两者都可以通过静脉储液器的高度来增加。 在第二号议定书中， 隔离RV扩大的直接影响，等容RV球囊将 使用时冠状静脉压保持恒定在0 mmHg。 在 此外，我们将尝试确定本地化和规模 心肌内冠状动脉电容（CIM）通过检查瞬态 冠状动脉流入道突然闭塞后心大静脉血流反应 孤立的狗心 假设冠状动脉模型（CEPI、RPRE、CIM、RPOST; CEPI =心外膜电容，RPRE = CIM前，RPOST = CIM后电阻）， CIM的本地化定义为RPOST/（RPRE + RPOST）。 这些 建立适当模型的基本信息， 了解冠状动脉循环的生理学。 的影响 血管舒张、左室前负荷改变和心肌僵硬对这些 将检查参数。 此外，我们将评估 冠状动脉电容对冠状动脉零流量压力的影响，以测试是否 冠状循环包含显著的Starling阻力（血管阻力 瀑布机制）。 这些研究应该有助于阐明 由此升高的右心充盈压改变了左心室和右心室 舒张功能和心肌灌注。

The myocardium is highly vascular and intramyocardial coronary vessels are able to store coronary blood inflow during diastole. Previously, little attention has been paid to the coronary venous system and coronary outflow pressure. However, if intramyocardial blood volume or capacitance is localized primarily in coronary veins, venules and capillaries, it is likely that coronary outflow (venous) pressure should be a major determinant of myocardial turgor and left ventricular (LV) diastolic distensibility, since changes in outflow pressure should be effectively transmitted to the microcirculation through the low venous resistance. Our overall goals are to assess the role of coronary venous pressure and intramyocardial blood storage: (a) as determinants of LV diastolic function, and; (b) in the regulation of coronary blood flow. Experiments will be performed in isolated, blood perfused dog hearts with the LV contracting isovolumically. We will assess the effect of coronary venous pressure on LV diastolic pressure-volume relations by comparing two protocols. In protocol I, right atrial and ventricular (RV) pressure will both be increased by the height of a venous reservoir. In protocol II, to isolate the direct effect of RV enlargement, an isovolumic RV balloon will be used with coronary venous pressure held constant at 0 mmHg. In addition, we will attempt to determine the localization and the magnitude of intramyocardial coronary capacitance (CIM) by examining a transient response great cardiac vein flow after sudden coronary inflow occlusion in isolated dog hearts. Assuming a coronary model (CEPI, RPRE, CIM, RPOST; CEPI=epicardial capacitance, RPRE=pre-CIM and RPOST=post-CIM resistance), the localization of CIM is defined by RPOST/(RPRE+RPOST). These fundamental information for constructing an adequate model for understanding the physiology of the coronary circulation. The effects of vasodilation, altered LV preload and myocardial stiffness on these parameters will be examined. In addition, we will assess the influence of coronary capacitance on coronary zero-flow pressure, to test whether the coronary circulation contains a significant Starling resistance (vascular waterfall mechanism). These studies should help elucidate mechanisms whereby elevated right heart filling pressures alter both left ventricular diastolic function and myocardial perfusion.