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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