Postsystolic shortening of acutely ischemic canine myocardium predicts early and late recovery of function after coronary artery reperfusion.
Postsystolic shortening of acutely ischemic canine myocardium predicts early and late recovery of function after coronary artery reperfusion.
复制标题
急性缺血犬心肌的收缩后缩短可预测冠状动脉再灌注后功能的早期和晚期恢复。
作者：
M. Takayama;R. M. Norris;Michael A. Brown;Lois C. Armiger;J. Rivers;H. D. White
缺血和缺血后心肌收缩后缩短和增厚是公认的现象，但其意义存在争议。为了探讨心肌收缩后收缩和增厚是否代表一种活跃的过程，并确定其在缺血恢复期间和恢复后功能恢复的可能预测指标的位置，我们在14只开胸麻醉犬(缺血90分钟，n=9；缺血180分钟，n=5)上，观察了缺血时收缩后收缩和增厚的幅度与冠脉阻断前同一节段的收缩后缩短和增厚的幅度或再灌注后30-60分钟和2-3周的收缩和增厚的幅度之间的相关性。在缺血开始后5min测量的心肌梗死前与收缩后缩短呈正相关(r=0.44，n=33，P<0.02)，与收缩后增厚呈正相关(r=0.73，n=13，P<0.01)。再灌注前即刻测量的收缩后缩短和增厚与恢复后2~3周的收缩后缩短和增厚之间也有很强的相关性(r=0.001.73，n=2 8；P<0.001.0 1；r=0.79，n=12；P<0.0 1)。在再灌流前即刻测量的收缩后缩短和增厚与再灌流后30-60min(“顿抑心肌”期间)早期恢复的收缩后缩短和增厚之间存在显著但不太确切的相关性。缺血90分钟的狗在再灌流后早期收缩后缩短和增厚持续存在，这预示着在2-3周后功能会进一步显著恢复。然而，发生180分钟缺血的狗在早期恢复期间没有出现收缩后缩短或增厚，并且在2-3周后没有表现出进一步的功能恢复。再灌注前即刻收缩后缩短和增厚的程度比缺血2-3周时缺血节段的组织学表现或缺血时血流的大小(15+/-3微米微球)更能预测功能的延迟恢复。根据再灌注前即刻和再灌注后功能恢复时的相关性，我们得出结论：收缩后收缩后收缩和运动障碍心肌节段增厚是其恢复潜力的标志。
Postsystolic shortening and thickening of ischemic and postischemic myocardium are well-recognized phenomena, but their significance is controversial. To discover whether postsystolic shortening and thickening might represent an active process and to establish their place as possible predictors of functional recovery during and after recovery from ischemia, we examined correlations in severely ischemic dyskinetic myocardial segments in 14 open-chest anesthetized dogs (90 minutes' ischemia, n = 9; 180 minutes' ischemia, n = 5) between the magnitudes of postsystolic shortening and thickening during ischemia and either the magnitudes of systolic shortening and thickening in the same segments before coronary occlusion or the magnitudes of shortening and thickening at 30-60 minutes and at 2-3 weeks after reperfusion. We found positive correlations between preocclusion shortening and postsystolic shortening (r = 0.44, n = 33 myocardial segments; p less than 0.02) and between preocclusion thickening and postsystolic thickening (r = 0.73, n = 13 segments; p less than 0.01), both measured at 5 minutes after onset of ischemia. Strong correlations were found also between postsystolic shortening and thickening measured immediately before reperfusion and systolic shortening and thickening measured after recovery at 2-3 weeks (r = 0.73, n = 28; p less than 0.001 for shortening; r = 0.79, n = 12; p less than 0.01 for thickening). Significant but less-exact correlations were found between postsystolic shortening and thickening measured immediately before reperfusion and early recovery of shortening and thickening at 30-60 minutes after reperfusion (during the "stunned myocardium" period). Postsystolic shortening and thickening persisted early after reperfusion in dogs that had had 90 minutes of ischemia, and this predicted further significant return of function at 2-3 weeks. However, dogs that had had 180 minutes of ischemia did not have postsystolic shortening or thickening during early recovery and showed no further return of function at 2-3 weeks. The magnitudes of postsystolic shortening and thickening immediately before reperfusion were better predictors of late return of function than the histological appearance of the ischemic segments at 2-3 weeks or the magnitude of their blood flow during ischemia (15 +/- 3 micron microspheres). From correlations made immediately before reperfusion with those at functional recovery after reperfusion, we conclude that postsystolic shortening and thickening of dyskinetic myocardial segments are markers of their potential for recovery.(ABSTRACT TRUNCATED AT 400 WORDS)