Abnormal myocardial fluid retention as an early manifestation of ischemic injury.
Abnormal myocardial fluid retention as an early manifestation of ischemic injury.
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心肌液体潴留异常是缺血性损伤的早期表现。
DOI：
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发表时间：
1976
期刊：
影响因子：
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通讯作者：
L. Buja
中科院分区：
文献类型：
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作者：
J. Willerson;F. E. Scales;A. Mukherjee;M. Platt;G. Templeton;G. Fink;L. Buja
57只离体、血液灌注、连续称重的犬心脏被用来研究早期心肌缺血损伤时异常心肌液体潴留的发展。将可膨胀球囊导管定位在54个心脏的左前降支冠状动脉（LAD）周围或3个心脏的近端左回旋支冠状动脉周围，用于研究以下冠状动脉闭塞间隔：a）10分钟后20分钟的再流，B）40分钟后无再流或20分钟的再流，以及c）60分钟无再流。固定冠状动脉闭塞60分钟后，组织学和超微结构检查显示许多缺血心肌细胞轻度肿胀，无间质水肿，心脏重量增加，细胞膜完整性明显结构缺陷。在冠状动脉闭塞40分钟和复流20分钟后，发生了显著的心脏重量增加，与缺血区域的特征性改变相关，包括广泛的间质性水肿和局灶性血管充血、出血和心肌细胞肿胀。还观察到细胞膜完整性的局灶性结构缺陷。LAD闭塞40分钟后发生的异常心肌液体潴留与缺血区钠-钾-ATP酶活性显著降低相关，但同一区域肌酸磷酸激酶或柠檬酸合酶活性无显著变化。尽管这些心脏中存在异常的心肌液体潴留，但在40分钟后冠状动脉闭塞解除后，腺苷和硝酸甘油输注可能难以扩张冠状动脉血管以维持持续的高冠状动脉流量，并且当腺苷和硝酸甘油输注延迟至复流后15分钟时，在闭塞解除后甚至超过初始充血流量值。因此，这些数据表明，受损的细胞体积调节和间质液积聚和细胞膜完整性的局灶性结构缺陷是缺血性损伤后再流的早期表现，但未能建立一个主要作用的异常液体潴留改变冠状动脉血流之前，广泛的心肌坏死的发展。相比之下，固定冠状动脉闭塞60分钟导致轻度细胞内肿胀，但没有显著的间质水肿，细胞膜完整性没有明显的结构缺陷。
Fifty-seven isolated, blood perfused, continuously weighed canine hearts have been utilized to study the development of abnormal myocardial fluid retention during early myocardial ischemic injury. Inflatable balloon catheters were positioned around the left anterior descending coronary arteries (LAD) of 54 hearts or the proximal left circumflex coronary arteries of three hearts for study of the following intervals of coronary occlusion: a) 10 minutes followed by 20 minutes of reflow, b) 40 minutes followed by either no reflow or by 20 minutes of reflow, and c) 60 minutes without reflow. After 60 minutes of fixed coronary occlusion, histologic and ultrastructural examination revealed mild swelling of many ischemic cardiac muscle cells in the absence of interstitial edema, cardiac weight gain, and obvious structural defects in cell membrane integrity. After 40 minutes of coronary occlusion and 20 minutes of reflow, significant cardiac weight gain occurred in association with characteristic alterations in the ischemic region, including widespread interstitial edema and focal vascular congestion and hemorrhage and swelling of cardiac muscle cells. Focal structural defects in cell membrane integrity were also noted. The development of abnormal myocardial fluid retention after 40 minutes of LAD occlusion occurred in association with a significant reduction in sodium-potassium-ATPase activity in the ischemic area, but with no significant alteration in either creatine phosphokinase or citrate synthase activity in the same region. Despite the abnormal myocardial fluid retention in these hearts, it was possible pharmacologically to vasodilate coronary vessels with adenosine and nitroglycerin infusion to maintain a consistently high coronary flow following release of the coronary occlusion after 40 minutes and to even exceed initial hyperemic flow values following release of the occlusion when adenosine and nitroglycerin infusion was delayed until 15 minutes after reflow. Thus, the data indicate that impaired cell volume regulation and interstitial fluid accumulation and focal structural defects in cell membrane integrity are early manifestations of ischemic injury followed by reflow, but fail to establish a major role for the abnormal fluid retention in altering coronary blood flow prior to the development of extensive myocardial necrosis. In contrast, fixed coronary occlusion for 60 minutes results in mild intracellular swelling but no significant interstitial edema and no obvious structural defects in cell membrane integrity.