Klocke F J, Mates R E, Canty J M, Ellis A K
Circ Res. 1985 Mar;56(3):310-23. doi: 10.1161/01.res.56.3.310.
On the basis of the material discussed, our current assessments of the controversial points mentioned at the beginning of this article may be summarized as follows: Pf = 0, the minimum back pressure to coronary flow associated with a measurable conductance, is indeed greater than coronary outflow pressure (and usually left ventricular diastolic pressure, as well). Pf = 0 needs to be taken into account in attempts to determine coronary driving pressure. In maximally vasodilated beds, Pf = 0 derived from diastolic pressure-flow relationships exceeds coronary outflow pressure by at least a few mm Hg. Pf = 0 varies with coronary outflow and/or diastolic ventricular cavity pressure. When left ventricular preload is elevated, Pf = 0 exceeds outflow pressure by increasing amounts. Pf = 0 appears to be systematically higher and pressure-dependent in beds in which vasomotor tone is operative. An improved understanding of the nature of, and basis for, time-dependent changes in resistance and/or Pf = 0 during long diastoles in nonvasodilated beds is needed. The contour of pressure-flow relationships which are free of reactive effects is curvilinear rather than linear. The degree of curvilinearity is substantial and can change with interventions. Curvilinearity is accentuated at lower pressures and may reflect changes in the number of perfused vascular channels as well as the caliber of individual channels. Capacitive effects need to be dealt with quantitatively in studies of pressure-flow relationships. Values of the capacitance which is involved in these effects vary with both pressure and tone. Capacitive flow also depends upon the instantaneous rate of change of pressure, which has not usually been defined in published studies. Although intramyocardial capacitance is large and plays an important role in systolic-diastolic flow interactions, a controlling role in diastolic coronary arterial pressure-flow relationships has not been established experimentally. In vasodilated beds, in-flow remains remarkably constant for several seconds after the brief transient associated with a step-change in the level of constant pressure perfusion during a long diastole. Calculations of coronary vascular resistance (by whatever method) remain of limited value, particularly when changes in response to an intervention are modest. Because of the curvilinear diastolic pressure-flow relationship, resistance is pressure-dependent and, at any given pressure, is probably best defined by establishing the slope of a diastolic pressure-flow curve which is free of reactive effects.(ABSTRACT TRUNCATED AT 400 WORDS)
基于所讨论的材料,我们目前对本文开头提及的争议点的评估可总结如下:与可测量的传导相关的冠状动脉血流的最小背压Pf = 0,确实大于冠状动脉流出压(通常也大于左心室舒张压)。在试图确定冠状动脉驱动压力时,需要考虑Pf = 0。在最大程度血管扩张的血管床中,由舒张压-血流关系得出的Pf = 0超过冠状动脉流出压至少几毫米汞柱。Pf = 0随冠状动脉流出压和/或舒张期心室腔压力而变化。当左心室前负荷升高时,Pf = 0超过流出压的幅度会增加。在存在血管舒缩张力的血管床中,Pf = 0似乎系统性地更高且与压力相关。需要更好地理解非血管扩张血管床在长舒张期内阻力和/或Pf = 0随时间变化的性质和基础。无反应性影响的压力-血流关系的轮廓是曲线而非直线。曲线程度相当大,并且会随干预而改变。曲线性在较低压力下更为明显,可能反映了灌注血管通道数量以及单个通道管径的变化。在压力-血流关系研究中,需要对电容效应进行定量处理。涉及这些效应的电容值随压力和张力而变化。电容性血流还取决于压力的瞬时变化率,而这在已发表的研究中通常未明确界定。尽管心肌内电容很大且在收缩期-舒张期血流相互作用中起重要作用,但在舒张期冠状动脉压力-血流关系中的控制作用尚未通过实验确定。在血管扩张的血管床中,在长时间舒张期内恒定压力灌注水平发生阶跃变化后的短暂瞬态之后,流入量会在几秒钟内保持相当恒定。冠状动脉血管阻力的计算(无论采用何种方法)价值有限,尤其是当对干预的反应变化较小时。由于舒张期压力-血流关系呈曲线,阻力与压力相关,并且在任何给定压力下,可能最好通过建立无反应性影响的舒张期压力-血流曲线的斜率来定义。(摘要截选至400字)