Avoidance of reperfusion injury after cardioplegia.

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Abstract
Myocardial damage incurred by ischemia appears during and seems to be accelerated by reperfusion, which restores recoverable cells and disrupts badly damaged ones. Vicious cycles of edema, Ca accumulation, acidosis, O2 toxicity, fibrillation and air, and platelet emboli contribute to the reperfusion injury. The philosophy of cool low pressure reperfusion gradually restoring temperature and pressure to normal is here contrasted experimentally with that of immediate normothermic, normotensive perfusion after 90 min. of ischemic cool, cardioplegic arrest. The preparation was a canine heart which was treated according to the usual clinical protocol except that 1 group was reperfused at normal temperature and pressure, and the other group started reperfusion cool; at a low pressure and over the next 10 min, pressure and temperature were restored to normal. Isovolumic ventricular function studies were done before ischemia and after recovery, and showed statistically significant differences between the groups in favor of the immediate restoration of normal temperature and pressure of perfusion. Contractile velocity and systolic pressure showed very highly significant (P = < 0.005) differences, wall stress-significant (P = < 0.025) and compliance-not-significant differences between the groups. Reperfusion with optimal conditions may prevent vicious cycle changes in ischemically damaged but recoverable myocardium. A step in this direction is reperfusion with blood at normal temperature and pressure rather than initially at lowered temperature and pressure.