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.
