Lawrence W E, Maughan W L, Kass D A
Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Md.
Circulation. 1992 Feb;85(2):816-27. doi: 10.1161/01.cir.85.2.816.
The mechanisms whereby reperfusion of a 20-minute coronary occlusion result in global functional recovery despite persistent regional dysfunction were studied in 11 open-chest reflex-blocked dogs.
Pressure-volume and pressure-thickness relations were simultaneously determined before, during, and after reperfusion of left anterior descending artery (LAD) occlusion. Wall thickness was determined by sonomicrometry in both ischemic and remote regions. Chamber systolic function was assessed by end-systolic pressure-volume relations (ESPVR) obtained by conductance catheter and defined by a slope (Ees) and volume shift at a common end-systolic pressure (delta Ves). LAD occlusion produced regional systolic thinning (-7 +/- 6%) and global left ventricular dysfunction (ESPVR shifted rightward (delta Ves = +8.6 +/- 5.1 ml, p less than 0.001) with no Ees change). After nearly 1 hour of reperfusion, LAD region thickening remained markedly reduced at 4 +/- 7% (versus 23 +/- 8%, control), yet chamber systolic function fully recovered (ESPVR shifted back leftward delta Ves = -8.9 +/- 6.5 ml). Ischemia induced a leftward shift and systolic thinning of LAD region pressure-thickness relations. Reperfusion returned end-systolic pressure-thickness relations halfway to their control position and diastolic relations fully to control position. This was primarily due to increased passive stiffening in about half the hearts and a partial return of active function in the remaining ones. The net effect was to eliminate systolic thinning over a physiological loading range, thus normalizing chamber systolic performance. Reflex activation, remote hyperfunction, or altered chamber loading did not account for the postreperfusion disparity between global and regional function.
These data suggest a mechanism to account for greater functional benefits of reperfusion beyond that anticipated from regional wall motion analysis.
在11只开胸并阻断反射的犬中，研究了冠状动脉闭塞20分钟后再灌注，尽管局部功能持续异常但整体功能得以恢复的机制。
在左前降支（LAD）闭塞前、闭塞期间及再灌注后，同时测定压力-容积和压力-厚度关系。通过超声测微法测定缺血区和远隔区的心肌厚度。通过电导导管获得的收缩末期压力-容积关系（ESPVR）评估心室收缩功能，其由斜率（Ees）和共同收缩末期压力下的容积变化（ΔVes）定义。LAD闭塞导致局部收缩期变薄（-7±6%）和整体左心室功能障碍（ESPVR右移（ΔVes = +8.6±5.1 ml，p<0.001），Ees无变化）。再灌注近1小时后，LAD区域增厚仍显著降低至4±7%（对照组为23±8%），但心室收缩功能完全恢复（ESPVR左移，ΔVes = -8.9±6.5 ml）。缺血导致LAD区域压力-厚度关系左移和收缩期变薄。再灌注使收缩末期压力-厚度关系恢复至对照位置的一半，舒张期关系完全恢复至对照位置。这主要是由于约一半心脏的被动僵硬度增加，其余心脏的主动功能部分恢复。净效应是在生理负荷范围内消除收缩期变薄，从而使心室收缩功能正常化。反射激活、远隔区功能亢进或心室负荷改变均不能解释再灌注后整体与局部功能之间的差异。
这些数据提示了一种机制，可解释再灌注带来的功能益处为何大于局部壁运动分析预期的益处。
