Journal of anesthesia
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Ischemic neuronal injury is characterized by early death mediated by excitotoxicity and by delayed death caused by apoptosis. Current evidence indicates that volatile agents, barbiturates, and propofol can protect neurons against ischemic injury caused by excitotoxicity. In the case of volatile agents and propofol, neuroprotection may be sustained if the ischemic insult is relatively mild; however, with moderate to severe insults, this neuronal protection is not sustained after a prolonged recovery period. ⋯ Cerebral ischemia is characterized by continued neuronal loss for a long time after the initial ischemic insult. Therefore, in investigations of cerebral ischemia, the duration of the recovery period should be taken into consideration in the analysis of the neuroprotective effects of anesthetic agents. A combination of different approaches that target specific stages of the evolution of ischemic injury may be required for sustained neuroprotection.
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Journal of anesthesia · Jan 2005
ReviewAnesthesia management for electroconvulsive therapy: hemodynamic and respiratory management.
Recent guidelines have stated that anesthesia for electroconvulsive therapy (ECT) should be administered by a specially trained anesthesiologist, and that anesthesiologists have overall responsibility, not only for anesthesia itself, but also for cardiopulmonary management and emergency care. Accordingly, anesthesiologists who administer anesthesia for ECT should have sufficient knowledge regarding the physiologically and pharmacologically unique effects of ECT. Electrical current during ECT stimulates the autonomic nervous system and provokes unique hemodynamic changes in systemic and cerebral circulation. ⋯ Reports of serious complications of this therapy are not frequent; however, patients with ischemic heart disease or cerebrovascular problems must be managed with special care to prevent myocardial infarction or neurological disorders. Safe physical management by anesthesiologists greatly contributes to the establishment of ECT under muscle relaxation. To maintain social confidence and to refine the therapy, anesthesiologists should play an essential role both in clinical activities and in laboratory research.
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Journal of anesthesia · Jan 2005
ReviewDrugs to facilitate recovery of neuromuscular blockade and muscle strength.
Several drugs that quicken recovery from neuromuscular blockade caused by vecuronium in anesthetized patients are reviewed. Ulinastatin, a protease inhibitor, is thought to promote the release of acetylcholine at the neuromuscular junction and increases hepatic blood flow and urine volume. For this reason, ulinastatin quickens recovery from neuromuscular blockade in anesthetized patients receiving vecuronium. ⋯ Therefore, recovery from neuromuscular blockade is hastened. Nicorandil enhances membrane K+ conductance in skeletal muscle and increases contraction of the skeletal muscle. Thus, nicorandil quickens recovery from neuromuscular blockade.