ZERO-FLOW PRESSURES AND PRESSURE-FLOW RELATIONSHIPS DURING SINGLE LONG DIASTOLES IN THE CANINE CORONARY BED BEFORE AND DURING MAXIMUM VASODILATION - LIMITED INFLUENCE OF CAPACITIVE EFFECTS
ZERO-FLOW PRESSURES AND PRESSURE-FLOW RELATIONSHIPS DURING SINGLE LONG DIASTOLES IN THE CANINE CORONARY BED BEFORE AND DURING MAXIMUM VASODILATION - LIMITED INFLUENCE OF CAPACITIVE EFFECTS
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DOI：
10.1172/jci110351
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发表时间：
1981-01-01
影响因子：
15.9
通讯作者：
ECHT, MP
中科院分区：
文献类型：
--
作者：
KLOCKE, FJ;WEINSTEIN, IR;ECHT, MP
在开胸犬的准备中，研究了舒张期冠状动脉血流受心肌内背压调节的建议，该背压大大超过冠状静脉和心室舒张压，在开胸犬的准备中，可以跟踪瞬时左回旋支压力和血流，直到在长时间的舒张期内流入停止。尽管r始终> 0.90，但在冠状动脉诱导的最大冠状动脉血管舒张之前和期间，单个冠状动脉内的压力-流量数据均凹向流量轴。在90%以上的病例中，二阶方程比线性方程拟合效果更好（P < 0.01）。二阶压力轴截距（Pf = 0）1平均为29 ± 1。血管舒张前为7（SD）mm Hg，2 mm Hg;左心房和右心房压力始终显著较低（8 . ±. 3和5 .+-。血管舒张前为2 mmHg，舒张后为8 ± 1 mmHg。2和4 .+-。1 mm Hg）。血管舒张前Pf = 0的值直接随冠状动脉流入压的水平而变化。对实验准备进行了修改，其中舒张期回旋支压可以保持恒定，用于评价长时间内测量的Pf = 0由于流入压降低时冠状动脉循环内的电容效应而导致误导性偏高的建议。Pf = 0时，电容效应引起的平均下降仅为5.9 ± 0.01。3.0舒张前为mmHg，舒张时为mmHg。Pf = 0显然是冠状动脉驱动压力和流量的重要定量决定因素，这是由与血管紧张度相关和独立的两个因素引起的。在改变生理情况期间的流量调整可能涉及Pf = 0以及冠状动脉阻力的显著变化。
The proposal that diastolic coronary flow is regulated by an intramyocardial back-pressure that substantially exceeds coronary venous and ventricular diastolic pressures was examined in an open-chest canine preparation in which instantaneous left circumflex pressure and flow could be followed to cessation of inflow during prolonged diastoles. Despite r being consistently > 0.90, pressure-flow data during individual diastoles were concave to the flow axis before and during pharmacologically induced maximum coronary vasodilation. Data were better fitted (P < 0.01) by 2nd-order equations than by linear equations in > 90% of cases. Second-order pressure-axis intercepts (Pf = 0)1 averaged 29 .+-. 7 (SD) mm Hg before vasodilation and 15 .+-. 2 mm Hg during vasodilation; left and right atrial pressures were always substantially lower (8 .+-. 3 and 5 .+-. 2 mm Hg before vasodilation and 8 .+-. 2 and 4 .+-. 1 mm Hg during dilation). Values of Pf = 0 before vasodilation varied directly with levels of coronary inflow pressure. A modification of the experimental preparation in which diastolic circumflex pressure could be kept constant was used to evaluate the suggestion that Pf = 0 measured during long diastoles are misleadingly high because of capacitive effects within the coronary circulation as inflow pressure decreases. Decreases in Pf = 0 attributable to capacitive effects averaged only 5.9 .+-. 3.0 mm Hg before vasodilation and were smaller during dilation. Pf = 0 apparently is a quantitatively important determinant of coronary driving pressure and flow, resulting from both factors related to, and independent of, vasomotor tone. Adjustments of flow during changing physiological situations may involve significant changes in Pf = 0 as well as in coronary resistance.