The effect of ischemic preconditioning and postconditioning on testicular torsion-detorsion injury

The primary pathophysiological event in testicular torsion is ischemia-reperfusion (I-R) injury, which is caused by the twisted spermatic cord and its release. Moreover, testicular torsion is most likely mediated by reactive oxygen species. Ischemic preconditioning (IPreC) is a phenomenon in which a prior ischemic stress renders the organ resistant to a subsequent ischemic insult. Ischemic postconditioning (IPostC) is defined as rapid intermittent interruptions of blood flow at the early phase of reperfusion, which mechanically alters reperfusion hydrodynamics. IPreC as well as IPostC provide powerful endogenous protection in many tissues against I-R injury. In this review, we explain the possible mechanisms involved in testicular I-R due to torsion-detorsion and aspects of IPreC and IPostC in the testis. IPreC is clinically feasible only when ischemia is predictable. However, unlike ischemia, reperfusion tends to have a more predictable onset. IPostC is a simple, harmless method that provides a new tool to protect organs from testicular I-R injury.