Avoidance of reperfusion injury after cardioplegia

Myocardial damage incurred by ischaemia appears during and seems to be accelerated by reperfusion, which restores recoverable cells and disrupts badly damaged ones. Vicious cycles of oedema, calcium accumulation, acidosis, oxygen 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 minutes of ischaemic cool, cardioplegic arrest. The preparation was a canine heart which was treated according to the usual clinical protocol except that one group was reperfused at normal temperature and pressure, and the other group started reperfusion cool and at a low pressure and over the next 10 minutes pressure and temperature were restored to normal. Isovolumic ventricular function studies were done before ischaemia and after recovery and showed statistically significant differences between the groups in favour of the immediate restoration of normal temperature and pressure of perfusion. Contractile velocity and systolic pressure showed very highly significant (p = less than 0.005) differences, wall stress significant (p = less than 0.025) and compliance not significant differences between the groups. Reperfusion with optimal conditions may prevent "vicious cycle" changes in ischaemically damaged but recoverable myocardium. We have shown that a step in this direction is reperfusion with blood at normal temperature and pressure rather than initially at lowered temperature and pressure.