Yuri Nakae

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BACKGROUND Activation of the mitochondrial adenosine triphosphate (ATP)-sensitive K+ channel (mitoK(ATP)) has been proposed as a critical step in myocardial protection by isoflurane-induced preconditioning in humans and animals. Recent evidence suggests that reactive oxygen species (ROS) may mediate isoflurane-mediated myocardial protection. In this study,(More)
Activation of the mitochondrial ATP-sensitive K+ channel (mitoKATP) and its regulation by PKC are critical events in preconditioning induced by ischemia or pharmaceutical agents in animals and humans. The properties of the human cardiac mitoKATP channel are unknown. Furthermore, there is no evidence that cytosolic PKC can directly regulate the mitoKATP(More)
VOLATILE anesthetics are well known to have cardio-protective effects similar to those of ischemic precondi-tioning, 1–11 but the mechanisms remain unclear. Recent evidence indicates that the protective effects of K ATP channel openers may be due to action on mitochondrial K ATP channels. 12–16 We have previously reported that 15 min of volatile anesthetic(More)
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