依普利酮对大鼠肥厚心肌缝隙连接蛋白重构及心电图指标变化的作用

目的观察白发性高血压大鼠(SHR)左心室心肌肥厚时心肌缝隙连接蛋白43(Cx43)和心电学指标的变化及依普利酮的作用。方法将24只SHR随机分为依普利酮治疗组(sHR-epl组,12只)、末治疗组(SHR-c组,12只),12只Wistar-Kyoto(WKY)大鼠作为正常血压对照组(正常组)。饲养10周(26周龄)后处死,用放射免疫法测定血浆和心脏组织醛固酮(ALD)浓度,体表心电图记录Q-Tc问期,免疫组化法观察大鼠心室肌Cx43分布特征。结果未治疗组血浆和心脏组织ALD高于对照组(均为P0.05),未治疗组Cx43表达(0.163±0.053)DM]较对照组(0.307±0.095)DM]明显减少(均为P0.01),且分布紊乱,同时伴Q-Yc间期延长;治疗组Cx43表达(0.288±0.089)DM]较末治疗组明显增多(P0.01),且分布规则,同时伴Q-Tc问期缩短。结论 SHR肥厚心肌存在Cx43重构现象,ALD升高可能导致肥厚心肌Cx43重构及心室肌除复极延长,依普利酮能有效改善Cx43重构及心室肌除复极时间。

Effects of eplerenone on gap junction remodeling and electrocardiographic parameters in hypertrophic myocardium

Objective To observe the changes of connexin 43 （ Cx43 ） and electrocardiographic parameters in hypertrophic left ventricle of spontaneously hypertensive rats （SHR） and the effect of eplerenone （Epl）. Methods Twenty-four male SHR were randomly divided into 2 groups ： SHR-epl group （ treated with Epl） , SHR-c group （hypertensive control）. Twelve male Wistar Kyoto rats （WKY） were selected as the normotensivc control. All rats were sacrificed after oral Epl once daily for 10 weeks. Aldosterone concentration in plasma and myocardial tissue were detected by radioimmunoassay. Electrocardiograms were recorded. The expression and distribution of Cx43 protein were detected by immunohistochemistry staining. Results The aldosterone concentration in plasma and myocardial tissue in SHR-c group were significantly higher than in WKY group （all P 〈0. 05）. The expression of Cx43 （0. 163±0. 053） DM] in SHR-c was significantly reduced compared to SHR-epl （0. 288±0. 089） DM] group （ all P 〈0. 01 ）, and disordered distribution was demonstrated and Q-Tc interval was prolonged in SHR-C group. Cx43 in SHR-epl group was in normal distribution. Conclusions Cx43 remodeling exists in myocardial hypertrophy in SHR. Plasma and tissue aldosterones play important roles in Cx43 remodeling and Q-Tc interval prolongation. Eplerenone can attenuate the action of Cx43 remodeling and Q-Tc interval prolongation in SHR.