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 = < 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 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.Myocardial damage appearing during reperfusion has been well-known from the earliest experience of cardioplegia as now used,' 2 and is acknowledged to be more dramatic than changes found in the ischaemic phase.3 Reperfusion accentuates the difference between recoverable and dubiously recoverable myocardium, making more obvious the damage previously only detectable by electron microscopy. The characteristic appearances of reperfusion injury result,24 6 with typical deterioration of function7-9 epitomised by "stiffness" of contraction and relaxation. Not only ischaemia but any withdrawal of metabolites or essential ions is followed by reperfusion injury on restoration of blood supply.The events which follow reperfusion are of the "vicious cycle" type. Oedema impairs the distribution and adequacy of perfusion by increasing the intramyocardial pressure and widening diffusion distances. The restoration of energy supply is further delayed by depressed mitochondrial function. High reperfusion pressures worsen the oedema but
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