ANESTHETIC NEUROPROTECTION AND CARDIAC PRECONDITIONING
Although inhalational agents have been suggested as contributing to neurotoxicity, they have also been shown to provide both neurologic and car-diac protective effects against ischemia-reperfusion injury. Ischemic preconditioning implies that a brief ischemic episode protects a cell from future, more pronounced ischemic events. Various molecular mechanisms have been suggested to protect cells preconditioned either through ischemic events or secondary to pharmacologic mechanisms, such as through the use of inhalational anesthetics. In the heart, preconditioning in part arises from actions at ATP-sensitive potassium (KATP) channels.
The exact mechanism of anesthetic precondi-tioning is likely to be multifocal and includes the opening of KATP channels, resulting in less mitochon-drial calcium ion concentration and reduction of reactive oxygen species (ROS) production. ROS are associated with cellular injury. For example, excit-atory NMDA receptors are linked to the development of neuronal injury. NMDA antagonists, such as the noble anesthetic gas Xenon, have been shown to be neuroprotective. Xenon has an anti-apoptotic effect that may be secondary to its inhibition of calcium ion influx following cell injury. Other inhalational agents, such as sevoflurane, have been shown to reduce markers of myocardial cell injury (eg, troponin T), compared with intravenous anesthetic techniques.
As with neurotoxicity, the role of inhalational anesthetics in tissue protection is the subject of ongoing investigation.
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