Roan P, Scales F, Saffer S, Buja L M, Willerson J T
J Clin Invest. 1979 Oct;64(4):1074-88. doi: 10.1172/JCI109546.
Characterization of the temporal evolution of resting segmental function and inotropic reserve after coronary occlusion may be important in evaluating attempts to salvage ischemic but non-necrotic myocardium. Accordingly, we chronically implanted up to six pairs of pulse-transit piezoelectric crystals in the left ventricular myocardium of dogs to measure segmental wall thickness. Segments were separated into groups according to the loss of net systolic thickening (NET) at 5 min postocclusion of the left anterior descending coronary artery in awake, unsedated dogs. Group 1 included segments with NET values of 67--100+ (percent control); group 2 between 67 and 0; and group 3 less than 0 (paradoxical motion). 5 min after coronary occlusion, group 1 NET was 92 +/- 5% (SEM) although significant decreases occurred in NET in group 2 (36 +/- 4%) and group 3 segments (-33 +/- 5%). Between 5 min and 24 h after coronary occlusion, no further significant changes occurred in NET in groups 1, 2, and 3 crystals. Some segments underwent further functional deterioration between 24 h and 1 wk after left anterior descending coronary artery occlusion, although no overall change occurred in segments with mild to moderate ischemic dysfunction. Segments with NET less than 0 at 24 h, on the other hand, exhibited a reduction in aneurysmal bulging between 24 h and 1 wk from -41 +/- 10 to -23 +/- 11% (n = 12, P = 0.02). Inotropic reserve was assessed with postextrasystolic potentiation (PESP) in 14 dogs, and with infusions of dopamine (11 dogs), and isoproterenol (13 dogs). PESP was the most potent intervention and produced a significant augmentation in NET in group 2 crystals at 1, 2, 4, 6,8, and 24 h after coronary occlusion but only at 1 and 2 h in NET in group 3 crystals. Thus, following experimental coronary occlusion, the evolution of ischemic segmental dysfunction is dynamic and variable. A significant degree of inotropic reserve, as assessed by PESP, dopamine, and isoproterenol, exists in segments with moderate ischemic dysfunction for 24 h but for only 2 h after coronary occlusion in those segments with the most severe ischemic dysfunction. In addition, at least some segmental sites with mild to moderate ischemic dysfunction at 24 h deteriorate further between 24 h and 1 wk after experimental coronary occlusion.
冠状动脉闭塞后静息节段功能和变力性储备的时间演变特征，对于评估挽救缺血但未坏死心肌的尝试可能具有重要意义。因此，我们在犬的左心室心肌中长期植入多达六对脉搏传输压电晶体，以测量节段壁厚。根据清醒、未镇静犬左前降支冠状动脉闭塞5分钟时净收缩期增厚（NET）的丧失情况，将节段分为几组。第1组包括NET值为67%-100%（对照百分比）的节段；第2组为67%至0%之间的节段；第3组小于0%（矛盾运动）。冠状动脉闭塞5分钟后，第1组的NET为92±5%（标准误），而第2组（36±4%）和第3组节段（-33±5%）的NET显著降低。冠状动脉闭塞后5分钟至24小时，第1、2、3组晶体的NET没有进一步的显著变化。在左前降支冠状动脉闭塞后24小时至1周之间，一些节段功能进一步恶化，尽管轻度至中度缺血性功能障碍的节段总体上没有变化。另一方面，24小时时NET小于0%的节段，在24小时至1周之间动脉瘤样膨出从-41±10%降至-23±11%（n = 12，P = 0.02）。在14只犬中用早搏后增强（PESP）评估变力性储备，在11只犬中用多巴胺输注评估，在13只犬中用异丙肾上腺素输注评估。PESP是最有效的干预措施，在冠状动脉闭塞后1、2、4、6、8和24小时使第2组晶体的NET显著增加，但仅在冠状动脉闭塞后1和2小时使第3组晶体的NET增加。因此，实验性冠状动脉闭塞后，缺血节段功能障碍的演变是动态且多变的。通过PESP、多巴胺和异丙肾上腺素评估，中度缺血性功能障碍的节段存在显著程度的变力性储备达24小时，但在最严重缺血性功能障碍的节段冠状动脉闭塞后仅存在2小时。此外，实验性冠状动脉闭塞后24小时至1周之间，至少一些24小时时轻度至中度缺血性功能障碍的节段部位进一步恶化。
