Geshi E, Sordahl L A, Ito S, Umetsu K, Katagiri T
Third Department of Internal Medicine, Showa University School of Medicine Tokyo, Japan.
Jpn Heart J. 1998 Nov;39(6):791-807. doi: 10.1536/ihj.39.791.
A canine model of postischemic myocardial dysfunction (15 min ischemia, 60 min reperfusion) was used to evaluate the relationship between energy metabolism and myocardial contractile function by on-line measurements of ECG, left ventricular pressure, coronary blood flow and regional segment shortening (%SS) with the continuous acquisition of 31PMR spectra. Two groups emerged from these studies; the first (n = 7) in which regional myocardial %SS remained significantly depressed after 60 min of reperfusion (stunned) and the second (n = 5) in which regional %SS returned to control levels after 60 min of reperfusion (non-stunned). Both groups exhibited rapid, similar decreases in %SS and parallel rapid decreases in the phosphocreatine to inorganic phosphate (PCr/Pi) ratio with the onset of ischemia. The PCr/ATP ratio exceeded control levels in the stunned group immediately upon reperfusion and remained significantly above control after 60 min of reperfusion. Measurements of tissue myocardial creatine kinase (CK) revealed a significant decrease in total tissue CK activity in stunned myocardium compared to control. A significant inverse relationship (r = -0.904, p < 0.003) was found between myocardial tissue CK specific activity and the PCr/ATP ratios. We postulate that the elevated PCr/ATP ratio caused by the impairment of energy transfer to the contractile apparatus constitutes a contractile dysfunction in the postischemic heart.
采用犬类缺血后心肌功能障碍模型(缺血15分钟,再灌注60分钟),通过在线测量心电图、左心室压力、冠状动脉血流量和区域节段缩短率(%SS),并连续采集31P MR谱,来评估能量代谢与心肌收缩功能之间的关系。这些研究产生了两组;第一组(n = 7),再灌注60分钟后区域心肌%SS仍显著降低(顿抑);第二组(n = 5),再灌注60分钟后区域%SS恢复到对照水平(非顿抑)。两组在缺血开始时均表现出%SS迅速、相似的下降,以及磷酸肌酸与无机磷酸(PCr/Pi)比值平行迅速下降。再灌注后,顿抑组的PCr/ATP比值立即超过对照水平,再灌注60分钟后仍显著高于对照。组织心肌肌酸激酶(CK)测量显示,与对照相比,顿抑心肌的总组织CK活性显著降低。心肌组织CK比活性与PCr/ATP比值之间存在显著的负相关关系(r = -0.904,p < 0.003)。我们推测,能量向收缩装置传递受损导致的PCr/ATP比值升高构成了缺血后心脏的收缩功能障碍。