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作 者:杨倩[1] 王立立[1] 田国栋 宋学莲 孟存良[1] YANG Qian;WANG Li-li;TIAN Guo-dong;SONG Xue-lian;MENG Cun-liang(Department of Cardiology,Hebei General Hospital,Shijiazhuang 050051,China;Department of Cardiology,Rongcheng People’s Hospital,Rongcheng 071600,China)
机构地区:[1]河北省人民医院心内科,河北石家庄050051 [2]容城县人民医院心内科,河北容城071600
出 处:《中国病理生理杂志》2019年第10期1884-1888,共5页Chinese Journal of Pathophysiology
摘 要:目的:探讨螺内酯(SP)对慢性房颤模型兔心房结构重构的影响及其可能的机制。方法:新西兰兔开胸后于左心房植入起搏电极,随机分为快速心房起搏组(RAP组)、螺内酯组(RAP+SP组)和假手术组(sham组)。RAP组和RAP+SP组持续心房起搏3周,分别给予安慰剂和螺内酯20 mg·kg^-1·d^-1灌胃,sham组不起搏,不给药。起搏前、后评价心房结构和功能,检测房颤诱发率;起搏后评价心房间质纤维化程度,检测心房胶原蛋白(collagen)Ⅰ、collagenⅢ、基质金属蛋白酶(MMP)-2和MMP-9的表达水平。结果:起搏3周后,与sham组相比,RAP组和RAP+SP组兔左心房明显扩张且伴收缩功能障碍;RAP+SP组与RAP组相比,左房结构和功能无明显差异。Sham组、RAP组和RAP+SP组各7只兔分别有0只、7只、5只诱发持续性房颤。与sham组相比,RAP组和RAP+SP组兔心房纤维化程度及collagenⅠ、collagenⅢ、MMP-2和MMP-9的蛋白表达水平明显增加;RAP+SP组与RAP组相比,心房纤维化程度和上述蛋白表达水平均下降(P<0.05)。结论:螺内酯能够抑制慢性房颤模型兔心房间质纤维化和胶原蛋白表达,抑制心房结构重构,这可能与螺内酯抑制心房MMP-2和MMP-9蛋白的表达有关。AIM:To evaluate the effects and potential mechanism of spironolactone(SP)on atrial structural remodeling in rabbit model of chronic atrial fibrillation(AF).METHODS:The sternotomy was performed and the pacing electrodes were fixed to the left atria of New Zealand white rabbits.The animals were randomly divided into 3 groups.The rabbits were subjected to rapid atrial pacing(RAP)for 3 weeks in RAP group(intragastric administration with placebo)and RAP+SP group(intragastric administration with spironolactone at 20 mg·kg^-1·d^-1),respectively.The rabbits in sham group did not receive RAP and drugs.Before and after RAP,the structure and function of the atria were evaluated and AF inducibility was tested.After RAP,the atrial fibrosis was evaluated,and the expression levels of collagen I,collagenⅢ,matrix metalloproteinase(MMP)-2 and MMP-9 were determined.RESULTS:After 3 weeks of RAP,compared with sham group,obvious left atrial enlargement and dysfunction were observed in RAP group and RAP+SP group,but those had no significant differences in these 2 groups.Sustained AF was induced in 7,5,and 0 rabbits in RAP group,RAP+SP group,and sham group,respectively.Compared with sham group,atrial interstitial fibrosis and the protein expression levels of collagenⅠ,collagenⅢ,MMP-2 and MMP-9 were all significantly increased in RAP group and RAP+SP group(P<0.05).Compared with RAP group,the the above indexes were all decreased in RAP+SP group(P<0.05).CONCLUSION:Spironolactone suppresses the atrial interstitial fibrosis and collagen expression,thus preventing atrial structural remodeling in rabbit model of chronic AF.The effect of spironolactone on reducing atrial MMP-2 and MMP-9 levels may be the potential mechanism.
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