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The effect of temporary periods of ischemia on the electrolytes and water of myocardial cells were studied in groups of mongrel dogs. Myocardial tissue exposed to 40 minutes of ischemia induced by occlusion of the circumflex branch of the left coronary artery developed no changes in water or electrolytes when compared to nonischemic left ventricle of the same or sham-operated animals, even though this period of ischemia is known to produce irreversible injury to many of the damaged cells. However, reperfusion of the affected myocardium with arterial blood for only 2 minutes resulted in striking increases in tissue H(2)O, Na(-), Cl(-) and Ca(2-). These changes in electrolytes increased in severity with longer periods of reflow, and tissue K(+) was decreased significantly after 10 minutes of reflow had passed. Analysis of the results suggested that the tissue edema was primarily the result of cellular swelling. Myocardium exposed to 15 minutes of ischemia followed by 2 minutes of reflow showed no significant changes aside from a slight increase in Na(+). These studies demonstrate that defects in cell volume regulation occur early in severe ischemic injury.

Changes produced in the posterior papillary muscle of the dog following 40 minutes of circumflex artery occlusion and 0 to 20 minutes of blood reflow were studied by electron miroscopy. With no reflow of blood, myocardial cells were modestly swollen, contained amorphous matrix densities in the mitochondria, had aggregation and margination of nuclear chromatin and relaxation of myofibrils. With as little as 2 minutes of blood reflow, cells developed contraction bands and were greatly swollen due to a generalized increase in sarcoplasmic space, formation of vacuoles and swelling of mitochondria. Frequently, cell membranes were lifted away from the myofibers, forming large subsarcolemmal blebs which appeared capable of compressing adjacent capillaries. The extracellular space did not appear to be enlarged, and the marked tissue edema found after reflow was due primarily to accumulation of intracellular fluid. In addition to explosive cell swelling, there was, over the 2- to 20-minute period of reflow, a progressive increase in size and number of granular mitochondrial dense bodies of the calcium accumulation type. No significant changes in lysosomes were observed. The speed with which the morphologic changes developed during very early reflow periods suggests that irreversible ischemic injury produces a defect in cell volume regulation during the phase of ischemia and that this defect becomes manifest if arterial flow is restored to the affected cells.