Heusch G, Schulz R
Abteilung für Pathophysiologie, Universitätsklinikum Essen.
Herz. 1999 Nov;24(7):509-14. doi: 10.1007/BF03044221.
During normoperfusion, both myocardial blood flow and contractile function are heterogeneously distributed throughout the left ventricle. Midwall segment shortening is greater at the apex than at the base of the left ventricle, and greater in the anterior than in the posterior wall. Also, transmural heterogeneity of myocardial deformation exists, with greater segment shortening and wall thickening in inner than in outer myocardial layers. Myocardial blood flow is greater in inner than in outer myocardial layers. Apart from transmural heterogeneities, there are adjacent regions with largely different resting flow in the same heart. While an increase in myocardial contractile function will lead to a metabolically mediated increase in myocardial blood, an increase in regional coronary perfusion within or above the autoregulatory range does not increase regional myocardial contractile function. During hypoperfusion induced by a proximal coronary stenosis, the reduction in subendocardial blood flow is more pronounced than that in subepicardial blood flow, and contractile function in the inner myocardial layers ceases more rapidly than in the outer myocardial layers. The reduced regional myocardial contractile function is closely matched to the reduced regional myocardial blood flow; however, such a coupling between reduced flow and function is lost when ischemia is prolonged for several hours in that function for a given flow is further reduced. Also, acute embolization of the coronary microcirculation induces a progressive loss of regional myocardial function at an unchanged regional myocardial blood flow, i.e. perfusion-contraction mismatch. During reperfusion, regional myocardial contractile function remains depressed for a prolonged period of time, depending on the severity, duration and location of the preceding ischemic episode, while regional myocardial blood flow is restored to almost normal. Recovery of contractile function in the outer myocardial layers is faster than in the inner myocardial layers.
在正常灌注期间,心肌血流量和收缩功能在整个左心室内呈非均匀分布。心尖部的室壁中层节段缩短大于左心室底部,前壁大于后壁。此外,心肌变形存在跨壁异质性,心肌内层的节段缩短和心肌增厚大于外层。心肌内层的血流量大于外层。除了跨壁异质性外,同一心脏中相邻区域的静息血流量也有很大差异。虽然心肌收缩功能的增加会导致代谢介导的心肌血流量增加,但在自动调节范围之内或之上的局部冠状动脉灌注增加并不会增加局部心肌收缩功能。在近端冠状动脉狭窄引起的灌注不足期间,心内膜下血流量的减少比心外膜下血流量的减少更明显,心肌内层的收缩功能比外层更快停止。局部心肌收缩功能的降低与局部心肌血流量的减少密切匹配;然而,当缺血持续数小时时,这种血流量减少与功能之间的耦合关系会丧失,因为在给定血流量下功能会进一步降低。此外,冠状动脉微循环的急性栓塞会导致局部心肌功能在局部心肌血流量不变的情况下逐渐丧失,即灌注-收缩不匹配。在再灌注期间,局部心肌收缩功能会在较长一段时间内持续抑制,这取决于先前缺血事件的严重程度、持续时间和位置,而局部心肌血流量几乎恢复正常。心肌外层收缩功能的恢复比内层更快。