Cardioprotective Effects of 17β-Estradiol Produced by Activation of Mitochondrial ATP-Sensitive K+Channels in Canine Hearts

摘要: Abstract We have previously demonstrated the effects of estrogen on modulation myocardial ATP-sensitive K + (K ATP ) channel. Previous studies that activation mitochondrial channel is a major contributor ischemic cardioprotection. The purpose present study was to investigate role in estrogen-induced protection after ischemia/reperfusion dogs. Anaesthetized dogs were subjected 60 min left anterior descending coronary artery occlusion followed by 2 h reperfusion. In first characterize sex and dose-response profile infarct size, drug intravenously administered at 10 or 20 μ g/kg. second cardioprotective mechanisms estrogen, vehicle, preconditioning 17 β -estradiol (10 g/kg) given, beginning 15 prior period presence absence 5-hydroxydecanoate (5-HD). study, administration resulted significant, dose-dependent limitation size. Estrogen provided similar magnitude both males females. size control animals averaged 39±5% risk region, compared with 14±5% region estrogen-treated 6±5% (both P v controls). Pretreatment 5-HD completely abolished preconditioning- limits infarction resulting from reperfusion fashion, irrespective gender difference. size-limiting effect estroge 5-HD, suggesting may result channels.