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Vol. 301, Issue 1, 234-240, April 2002
-Estradiol on Reperfusion
Arrhythmias and Infarct Sizes in Canine Hearts
Departments of Surgery (C.-H.T.) and Internal Medicine (T.-M.L.),
Cardiology Section, National Taiwan University College of Medicine,
National Taiwan University Hospital, Taipei, Taiwan; College of
Medicine (S.-F.S.), National Cheng Kung University, Tainan, Taiwan; and
Department of Surgery (T.-F.C.), Municipal Jen-Ai Hospital, Taipei,
Taiwan
We have demonstrated the effects of estrogen on modulation of
ATP-sensitive K+ channels; however, the subcellular
location of these channels is unknown. The purpose of the present study
was to investigate the role of the sarcolemmal and mitochondrial
ATP-sensitive K+ channels in a canine model of myocardial
infarction after stimulation with 17
-estradiol. Anesthetized dogs
were subjected to 60 min of the left anterior descending coronary
artery occlusion followed by 3 h of reperfusion. Infarct size was
markedly reduced in estradiol-treated dogs compared with controls
(14 ± 6 versus 42 ± 6%, P < 0.0001), indicating the effective dose of estradiol administrated. Pretreatment with the mitochondrial ATP-sensitive K+ channel antagonist
5-hydroxydecanoate completely abolished estradiol-induced cardioprotection. The sarcolemmal ATP-sensitive K+ channel
antagonist
1-15-12-(5-chloro-o-anisamido)ethyl-methoxyphenyl)sulfonyl-3-methylthiourea (HMR 1098) did not significantly attenuate estradiol-induced
infarct size limitation. In addition, estradiol administration
significantly reduced the incidence and duration of reperfusion-induced
ventricular tachycardia and ventricular fibrillation. Although
5-hydroxydecanoate alone caused no significant effect on the incidence
of reperfusion arrhythmias in the presence or absence of estradiol, the
administration of HMR 1098 abolished estrogen-induced improvement of
reperfusion arrhythmias. Pretreatment with the estrogen-receptor
antagonist faslodex (ICI 182,780) did not alter estrogen-induced
infarct-limiting and antiarrhythmic effects. These results demonstrate
that estrogen is cardioprotective against infarct sizes and fatal
reperfusion arrhythmias by different ATP-sensitive K+
channels for an estrogen receptor-independent mechanism. The infarct
size-limiting and antiarrhythmic effects of estrogen were abolished by
5-hydroxydecanoate and HMR 1098, suggesting that the effects may result
from activation of the mitochondrial and sarcolemmal ATP-sensitive
K+ channels, respectively.
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