Medical gas research
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Medical gas research · Jan 2012
Propofol and magnesium attenuate isoflurane-induced caspase-3 activation via inhibiting mitochondrial permeability transition pore.
The inhalation anesthetic isoflurane has been shown to open the mitochondrial permeability transition pore (mPTP) and induce caspase activation and apoptosis, which may lead to learning and memory impairment. Cyclosporine A, a blocker of mPTP opening might attenuate the isoflurane-induced mPTP opening, lessening its ripple effects. Magnesium and anesthetic propofol are also mPTP blockers. We therefore set out to determine whether propofol and magnesium can attenuate the isoflurane-induced caspase activation and mPTP opening. ⋯ These data illustrate that Mg2+ and propofol may ameliorate the isoflurane-induced neurotoxicity by inhibiting its mitochondrial dysfunction. Pending further studies, these findings may suggest the use of Mg2+ and propofol in preventing and treating anesthesia neurotoxicity.
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Volatile anesthetics are one class of the most commonly used drugs. However, the mechanisms for these drugs to induce anesthesia are not fully understood and have been under intensive investigation. Two other effects of these anesthetics on the central nervous system, volatile anesthetics-induced neuroprotection and neurotoxicity, currently are hot research fields. ⋯ In this regard, the contribution of general anesthesia/anesthetics to postoperative cognitive decline, a clinical entity whose existence has been supported by substantial evidence, also has not been established. This paper will be focused on reviewing the evidence, especially the clinical evidence, for volatile anesthetics-induced neuroprotection and neurotoxicity. Efforts will be devoted to facilitating the understanding of the two seemingly contradictory effects of these important drugs on the brain.