Abstract
Stasis in the coronary microcirculation has been proposed as a major factor leading to left ventricular subendocardial hemorrhagic necrosis and low-output syndrome after open-heart operations. In order to test this proposition, anoxic arrest of 60 to 75 minutes' duration was produced in two groups of experimental animals. The control animals all died intraoperatively, while all those whose left coronary artery was flushed with a physiological solution during the experiment survived the procedure without significant hemodynamic or pathological changes. From this and a review of the literature, proposals are advanced on the cause of hemorrhagic necrosis and the protection afforded by coronary flushing during anoxic cardioplegia.
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