The (still) unknown mechanism of ischemic preconditioning: possible involvement of reduced Na⁺/H⁺ exchange

Conclusion

These observations support the view that the mechanism responsible for the anti-infarct effect of ischemic preconditioning is far from being completely understood. The potential involvement of reduced Na⁺/H⁺ exchange in this effect cannot be ruled out on the basis of currently available, information and illustrates the uncompletness of our knowledge of the molecular mechanisms responsible for the cardioprotective effect of preconditioning. The potential role of attenuated Na⁺/H⁺ exchange in this effect cannot be easily integrated into the signal cascade of messengers proposed for preconditioning, but may be seen as a mechanism acting in parallel. The importance of this mechanism may depend on the conditions, as initial glycogen content or alternative routes of Na⁺ gain. These conditions may be different in the isolated crystalline perfused heart as compared toin situ myocardium. Further studies are necessary to resolve the possible role of attenuated acidosis and Na⁺/H⁺ exchange in ischemic preconditioning. These studies should aim to dissociate glycogen depletion, attenuated acidosis, and reduced Na⁺/H⁺ exchangein situ preconditioned myocardium.