Myocardial preconditioning and cardioprotection by volatile anaesthetics.

The biological bases and the clinical applications of ischaemic and anaesthetic preconditioning are reviewed. Ischaemic preconditioning is an endogenous defensive phenomenon of the myocardium in which brief periods of ischaemia followed by reperfusion reduce the infarct size induced by longer ischaemic stimuli; both an early and a late phase may be distinguished. In the early phase, the mediators released activate ATP-dependent potassium channels and kinase cascade; these enzymes migrating at the level of various subcellular structures phosphorylate some end-effectors responsible for cardioprotection. Several molecules that are involved in the regulation of cell death during ischaemia-reperfusion injury have been proposed for such a role, including mitochondrial ATP-dependent potassium channels, connexins and cytoskeletal and mitochondrial proteins. In the late phase, the triggers and mediators themselves, plus nitric oxide, are responsible for the genetic reprogramming providing a protective effect via ex-novo synthesis of proteins. Volatile halogenated anaesthetics may induce a particular sort of pharmacological preconditioning, anaesthetic preconditioning, which presents some differences in the biochemical signalling mechanism but is able to give protection comparable to the ischaemic form. Anaesthetic preconditioning presents obvious advantages compared to ischaemic preconditioning, and researchers have tried to take advantage of this in the clinical setting, in cardiac surgical patients, in neuroprotection and to prolong the survival of organs destined for transplantation.