Effects of isoflurane on ischemia-reperfusion injury in organ Mechanism of protective effect of.docVIP
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Effects of isoflurane on ischemia-reperfusion injury in organ Mechanism of protective effect of
PAGE \* MERGEFORMAT 24
Effects of isoflurane on ischemia-reperfusion injury in organ Mechanism of protective effect of
In recent years, with the clinical thrombolytic therapy, catheterization, arterial bypass surgery, cardiac recovery, cardiac bypass surgery, limb replantation and organ transplants and other methods of establishing and promoting the application of ischemia in many tissues and organs obtained by the blood reperfusion. Ischemia-reperfusion injury (ischemia reperfusion injury.IRI) refers to the post-ischemic reperfusion not only fail to make tissues and organs function recovery, but increased tissue and organ dysfunction and structural damage. To explore the characteristics of ischemia-reperfusion injury, laws, and the mechanism has become a hot spot of today’s medical research. Represented by isoflurane volatile inhalation anesthetics for many organs, ischemia-reperfusion injury with a cellular level, multi-organ protective effect, its protection mechanism is not yet entirely clear, but now at home and abroad so far carried out by many of the studies have fully demonstrated the class of drugs with a clear protective effect of multiple organ, now its protection mechanisms are summarized below:
A mechanism of myocardial protection
1.1 Activation of mitochondrial ATP-sensitive potassium channel (KATP)
Mitochondrial ATP-sensitive potassium channel (KATP) commonly found in the myocardium and coronary blood vessels, in the protection of myocardial ischemia-reperfusion injury plays an important role. Isoflurane could act on cardiac adenosine A1 receptors on the cell membrane, activating ATP-sensitive potassium channels [1]. Isoflurane may directly activate the KATP channel, does not depend on adenosine, protein kinase C, tyrosine kinase, p38 mitogen-activated protein kinase, etc. [2]. KATP channel opening, K outflows, weakening the cell membrane depolarization and shorten the cardiac action potential duration ((APD), thereby reducin
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