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阿托伐他汀對慢性兔房顫模型心房電重構(gòu)的影響

發(fā)布時間:2018-07-16 16:00
【摘要】:目的:通過快速起搏心房3周建立慢性兔房顫模型,探討阿托伐他汀(ATO)對該模型心房電重構(gòu)的影響及其可能機制。方法:將24只新西蘭大白兔開胸,于左心房植入起搏和測試電極,隨機分為3組:模型(model)組和ATO組持續(xù)心房起搏3周,分別給予安慰劑和阿托伐他汀2.5 mg·kg~(-1)·d~(-1)灌胃;假手術(shù)(sham)組不起搏,不給藥。起搏前后用電生理刺激儀檢測心率、P波寬度、心房有效不應(yīng)期(AERP)和房顫誘發(fā)率的變化;起搏后采用Western blot檢測心房Cav1.2、Kv4.3和髓過氧化物酶(MPO)的蛋白表達水平。結(jié)果:Sham組、model組和ATO組分別有0、5和4只兔誘發(fā)持續(xù)性房顫。起搏3周后,與sham組相比,model組和ATO組兔心率和P波寬度均增加,AERP縮短(P0.05);ATO組與model組相比,AERP增加(P0.05),心率和P波寬度無明顯變化。與sham組相比,model組和ATO組兔心房Cav1.2和Kv4.3的蛋白表達水平下降,MPO的蛋白表達水平升高(P0.05);ATO組與model組相比,Cav1.2的表達增加,MPO的表達下降(P0.05),Kv4.3無明顯變化。結(jié)論:阿托伐他汀能夠通過抑制慢性兔房顫模型心房Cav1.2蛋白表達下降和AERP的縮短,抑制心房電重構(gòu),其潛在機制可能是阿托伐他汀抑制了心房MPO蛋白的高表達。
[Abstract]:Aim: to investigate the effect of Atto vastatin (ATO) on atrial electrical remodeling in rabbit atrial fibrillation model with rapid atrial pacing for 3 Zhou Jianli. Methods: Twenty-four New Zealand white rabbits were divided into three groups randomly: the model group and the ATO group were given placebo and Atto vastatin 2.5 mg kg ~ (-1) d ~ (-1) for 3 weeks of continuous atrial pacing. No pacing or medication was given in (sham) group. The changes of heart rate P wave width, atrial effective refractory period (AERP) and atrial fibrillation evoked rate were detected by electrophysiological stimulator before and after pacing, and the protein expression of Cav1.2 Kv4.3 and myeloperoxidase (MPO) were detected by Western blot after pacing. Results 5 rabbits and 4 rabbits in the control group and ATO group induced persistent atrial fibrillation, respectively. After 3 weeks of pacing, compared with sham group, the heart rate and P-wave width of model group and ATO group increased significantly (P0.05), while the heart rate and P-wave width of ATO group increased compared with model group (P0.05), but the heart rate and P-wave width did not change significantly. Compared with sham group and ATO group, the expression level of Cav1.2 and Kv4.3 in rabbit atrium were decreased (P0.05). Compared with model group, the expression of Cav1.2 increased in ATO group (P0.05). Conclusion: Atto can inhibit atrial electrical remodeling by inhibiting the decrease of atrial Cav1.2 protein expression and the shortening of atrial electrical remodeling in chronic rabbit atrial fibrillation model. The underlying mechanism may be that Atto vastatin inhibits the high expression of atrial Cav1.2 protein.
【作者單位】: 河北省人民醫(yī)院心內(nèi)科;河北省人民醫(yī)院腎內(nèi)科;
【分類號】:R-332;R541.75

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