Vis M A, Sipkema P, Westerhof N
Laboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit, Amsterdam, The Netherlands.
Am J Physiol. 1997 Mar;272(3 Pt 2):H1516-26. doi: 10.1152/ajpheart.1997.272.3.H1516.
Pressure-flow relations were calculated for a symmetrical, maximally dilated, crystalloid-perfused coronary vascular network embedded in cardiac muscle in (static) diastole and (static) systole at two muscle lengths: slack length and 90% of maximal muscle length (Lmax). The calculations are based on the "time-varying elastance concept." That is, the calculations include the mechanical properties of the vascular wall and the (varying) mechanical properties of the myocardial tissue (in cross-fiber direction). We found that, at any given perfusion pressure, coronary flow is smaller in systole than in diastole. Relative reduction in vascular cross-sectional area, which forms the basis of flow impediment, was largest for the smallest arterioles. At a constant perfusion pressure of 62.5 mmHg, the transition from (static) diastole to (static) systole at constant muscle length ("isometric contraction") was calculated to reduce flow by 74% (from 18.9 to 5.0 ml x min(-1) x g(-1)) and by 64% (from 12.6 to 4.6 ml x min(-1) x g(-1)) for the muscle fixed at slack length and 90% of Lmax, respectively. At this perfusion pressure, contraction with 14% shortening (from 90% of Lmax in diastole to slack length in systole) was calculated to reduce flow by 61% (from 12.6 to 5.0 ml x min(-1) x g(-1)). Increasing muscle length from slack length to 90% of Lmax decreases coronary flow by 34% in diastole and by 8% in systole. We conclude that modeling cardiac contraction on the basis of the time-varying elastic properties of the myocardial tissue can explain coronary flow impediment and that contractions, with or without shortening, have a larger effect on coronary flow than changes in muscle length.
在心肌处于（静态）舒张期和（静态）收缩期时，针对嵌入心肌中的对称、最大扩张、晶体灌注的冠状动脉血管网络，在两个肌肉长度下计算压力 - 流量关系：松弛长度和最大肌肉长度（Lmax）的90%。这些计算基于“时变弹性概念”。也就是说，计算包括血管壁的力学特性以及心肌组织（跨纤维方向）的（变化的）力学特性。我们发现，在任何给定的灌注压力下，收缩期的冠状动脉血流量都比舒张期小。形成血流阻碍基础的血管横截面积的相对减小，对于最小的小动脉来说是最大的。在62.5 mmHg的恒定灌注压力下，对于固定在松弛长度和Lmax的90%的肌肉，在恒定肌肉长度下从（静态）舒张期到（静态）收缩期的转变（“等长收缩”）经计算可使血流量分别减少74%（从18.9降至5.0 ml·min⁻¹·g⁻¹）和64%（从12.6降至4.6 ml·min⁻¹·g⁻¹）。在该灌注压力下，缩短14%（从舒张期的Lmax的90%到收缩期的松弛长度）的收缩经计算可使血流量减少61%（从12.6降至5.0 ml·min⁻¹·g⁻¹）。将肌肉长度从松弛长度增加到Lmax的90%，在舒张期可使冠状动脉血流量减少34%，在收缩期减少8%。我们得出结论，基于心肌组织的时变弹性特性对心脏收缩进行建模可以解释冠状动脉血流阻碍，并且收缩（无论有无缩短）对冠状动脉血流的影响比肌肉长度变化更大。
