Activation of Mitochondrial ATP-Sensitive Potassium Channel Contributes to Protective Effect in Prolonged Myocardial Preservation.
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Guo W, Chen N, Chen Y, Xia Q, Shen Y
Activation of Mitochondrial ATP-Sensitive Potassium Channel Contributes to Protective Effect in Prolonged Myocardial Preservation.
Conf Proc IEEE Eng Med Biol Soc. 2005;4:4027-30.
- PubMed ID
- 17281115 [ View in PubMed]
- Abstract
To find a better strategy for effective donor organ preservation, here we used a model of long-term hypothermia preservation of rat hearts to investigate the cardioprotective effects of diazoxide, a selective opener of mitochondrial ATP-sensitive potassium channel (mitoKATP ). Cardiac function was impaired by 8-hour ischemic preservation following 30 minutes of reperfusion. Treatment with diazoxide significantly attenuated the decline of myocardial contractility, and decreased the lactate dehydrogenase leakage and myocardial edema. Diazoxide also prevented the loss of activity of mitochondrial superoxide dismutases and sarcolemmal Na+/K+ ATPase during ischemia or reperfusion period, respectively. These effects of diazoxide could be abolished by a selective mitoKATp blocker 5-hydroxydecanoate. The results suggest that diazoxide, as a supplementation in cardioplegic solution, could enhance myocardial protection by opening mitoKATp channel, and better maintenance of mitochondrial anti-oxidative enzyme.
DrugBank Data that Cites this Article
- Drug Targets
Drug Target Kind Organism Pharmacological Action Actions Diazoxide ATP-sensitive inward rectifier potassium channel 11 Protein Humans YesInducerDetails