ABNORMAL MYOCARDIAL FLUID RETENTION AS AN EARLY MANIFESTATION OF ISCHEMIC-INJURY

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 87  (1) , 159-188
Abstract
Isolated, blood perfused, continuously weighed dog hearts (57) were 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 3 hearts for study of the following intervals of coronary occlusion: 10 min followed by 20 min of reflow, 40 min followed by either no reflow or by 20 min of reflow and 60 min without reflow. After 60 min 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 min of coronary occlusion and 20 min 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 noted. The development of abnormal myocardial fluid retention after 40 min of LAD occlusion occurred in association with a significant reduction in Na-K-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 min and to even exceed initial hyperemic flow values following release of the occlusion when adenosine and nitroglycerin infusion was delayed until 15 min after reflow. 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. Fixed coronary occlusion for 60 min results in mild intracellular swelling but no significant interstitial edema and no obvious structural defects in cell membrane integrity.