Haendchen R V, Ong K, Fishbein M C, Zwehl W, Meerbaum S, Corday E
Circ Res. 1985 Nov;57(5):718-28. doi: 10.1161/01.res.57.5.718.
This study tests the hypothesis that ischemic but viable reperfused myocardium can be differentiated from infarcted reperfused myocardium by regional analysis of myocardial echo amplitudes. In eight closed-chest, anesthetized dogs, the left anterior descending coronary artery was occluded for 3 hours, followed by 1 hour of reperfusion, and sacrifice. Infarct size was measured by the triphenyl tetrazolium chloride technique in a 1-cm-thick mid-left ventricular transverse slice, and matched with a corresponding end-diastolic two-dimensional echo short-axis cross-section. Outlining of epi- and endocardial surfaces, along with construction of a mid-myocardial outline, allowed measurements of regional myocardial echo intensities and grey-level histograms in subendo- and subepicardial regions. In 36 eventually infarcted subendocardial segments (greater than 20% wall necrosis), average pixel intensity (arbitrary units) was 73.7 +/- 33.1 (SD) in control, 75.8 +/- 33.0 at 3 hours of occlusion, and 107.8 +/- 40.9 at 5 minutes, 105.5 +/- 38.9 at 15 minutes, and 101.1 +/- 37.6 at 60 minutes postreperfusion P less than 0.05 vs. control or occlusion); intensity in normal segments (no or less than 20% wall necrosis) was 60.0 +/- 18.6 in control, 57.4 +/- 20.3 at 3 hours of occlusion, and 63.5 +/- 14.8, 68.0 +/- 27.9, and 64.2 +/- 22.3 at 5, 15, and 60 minutes postreperfusion, respectively (no significant change). The skew of the grey-level distribution in infarcted subendocardial segments did not change from control (0.49 +/- 0.72) to 3 hours of occlusion (0.41 +/- 0.52), but decreased (shift to higher echo amplitude) significantly at 5 minutes (-0.31 +/- 0.53), 15 minutes (-0.22 +/- 0.50), and 60 minutes (-0.28 +/- 0.45) after reperfusion (P less than 0.05 vs. control or occlusion); in normal subendocardial segments, there was no significant change throughout the study. In 31 partly infarcted subepicardial segments (greater than 50% wall necrosis), changes in postreperfusion echo amplitudes were less significant. Average pixel intensity was 71.3 +/- 28.6 in control, 71.8 +/- 29.2 after coronary occlusion, and 89.2 +/- 35.3, 83.7 +/- 37.5, and 85.6 +/- 34.9 at 5, 15, and 60 minutes after reperfusion, respectively. It is concluded that reperfusion of irreversibly injured myocardium is associated with consistent early increase in regional myocardial echo intensities and changes in the grey-level distribution. Such alterations might be used to detect the extent of tissue necrosis within minutes after reperfusion.
通过对心肌回声幅度进行区域分析，可将缺血但存活的再灌注心肌与梗死的再灌注心肌区分开来。在八只开胸麻醉的犬中，左前降支冠状动脉闭塞3小时，随后再灌注1小时，然后处死动物。梗死面积通过三苯基氯化四氮唑技术在左心室中部1厘米厚的横向切片中测量，并与相应的舒张末期二维超声短轴横截面进行匹配。勾勒心外膜和心内膜表面，并构建心肌中层轮廓，可测量心内膜下和心外膜下区域的局部心肌回声强度和灰度直方图。在36个最终梗死的心内膜下节段（壁坏死大于20%）中，对照时平均像素强度（任意单位）为73.7±33.1（标准差），闭塞3小时时为75.8±33.0，再灌注后5分钟为107.8±40.9，15分钟为105.5±38.9，60分钟为101.1±37.6（与对照或闭塞相比，P<0.05）；正常节段（无壁坏死或壁坏死小于20%）对照时强度为60.0±18.6，闭塞3小时时为57.4±20.3，再灌注后5、15和60分钟分别为63.5±14.8、68.0±27.9和64.2±22.3（无显著变化）。梗死心内膜下节段灰度分布的偏度从对照时的0.49±0.72到闭塞3小时时的0.41±0.52没有变化，但在再灌注后5分钟（-0.31±0.53）、15分钟（-0.22±0.50）和60分钟（-0.28±0.45）显著降低（向更高回声幅度转变）（与对照或闭塞相比，P<0.05）；在心内膜下正常节段，整个研究过程中无显著变化。在31个部分梗死的心外膜下节段（壁坏死大于50%）中，再灌注后回声幅度的变化不太显著。对照时平均像素强度为71.3±28.6，冠状动脉闭塞后为71.8±29.2，再灌注后5、15和60分钟分别为89.2±35.3、83.7±37.5和85.6±34.9。结论是，不可逆损伤心肌的再灌注与局部心肌回声强度的持续早期增加和灰度分布的变化相关。这种改变可用于在再灌注后数分钟内检测组织坏死的程度。
