• B Preckel, J Müllenheim, and W Schlack.
• Klinik für Anaesthesiologie, Universitätsklinikums Düsseldorf. preckel@med.uni-duesseldorf.de
• Anaesthesiol Reanim. 2002 Jan 1; 27 (5): 116-23.

AbstractMyocardial ischaemia/reperfusion situations may occur during the perioperative period. The cardioprotective effects of anaesthetics have been known for a long time: volatile anaesthetics reduce the ischaemic cell damage and infarct development. Besides ischaemia, reperfusion itself can also lead to cellular damage, thereby further increasing the ischaemic injury (reperfusion injury). Inhalational anaesthetics offer specific protective effects against reperfusion injury in isolated hearts as well as in rabbit hearts in vivo. This protection does not depend on haemodynamic side-effects of the substances and is even present after protecting the heart against ischaemic damage using a cardioplegic solution. Short periods of ischaemia render the myocardium resistant to subsequent longer periods of ischaemia. This strongest endogenous protective mechanism against the consequences of an ischaemia is known as ischaemic preconditioning. The protective effect can also be produced by stimulation of different types of receptors: the respective agonists produce pharmacological (chemical) preconditioning. The common pathway of the signal transduction cascade of both ischaemic and chemical preconditioning includes the sarcolemnal and/or mitochondrial ATP-sensitive potassium channel. Volatile anaesthetics can imitate the protective effects of a short ischaemia, thereby producing chemical preconditioning. This effect depends, at least in part, on anaesthetic-induced opening of ATP-sensitive potassium channels.

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