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作 者:郭再萍[1] 石国平[1] 郭江宏[1] 徐琴[1] 沈建宏[1] 马根山[2]
机构地区:[1]如皋市人民医院心内科,江苏如皋226500 [2]东南大学附属中大医院心内科,江苏南京210009
出 处:《东南大学学报(医学版)》2010年第5期528-531,共4页Journal of Southeast University(Medical Science Edition)
基 金:南通市科技局指导性项目(S9930)
摘 要:目的:探讨螺内酯预处理对兔心肌梗死(心梗)早期非梗死区冠脉内皮内皮型一氧化氮合酶(eNOS)表达及血流动力学的影响。方法:将24只雄性新西兰大耳白兔随机分为A、B、C 3组,A、B组予饲喂高脂饲料,C组饲喂普通饲料;A组予螺内酯(20 mg.kg-1.d-1)口服4周,结扎前降支复制急性心梗模型。测定术前及术后血醛固酮(Aldo)浓度及结扎近心段冠脉内皮eNOS表达情况,测定左室的血流动力学变化并加以比较。结果:A、B组eNOS表达均弱于C组,而A组高于B组(均P<0.05);A、B两组术后血Aldo浓度明显高于C组(P<0.05),A、B组间比较差异无显著性(P>0.05);A、B两组左室平均收缩压(MSP)、平均舒张压(MDP)、平均动脉压(MAP)及左室等容收缩功能(+dp/dt max)明显高于C组(P<0.05),而A组左室MSP、+dp/dt max的变化值又均高于B组(P<0.05)。结论:螺内酯可使非梗死区冠脉内皮eNOS表达增强;螺内酯可以改善心梗早期的血流动力学状态,具体机制可能与其能协同Aldo的非基因组作用促进非梗死区冠脉扩张有关。Objective: To investigate the effect of spironlactone on the expression of endothelial nitric oxide synthase(eNOS) in rabbit coronary artery of non-infarcted area and the hemodynamics in the early period of acute myocardial infraction( AMI ). Methods: 24 male rabbits were divided into three groups (A, B, C ) randomly. Rabbits in group A and B were both fed with high fat diet for four weeks, and those in group A were fed with spironolactone (20mg·kg^-1·d^-1) at the same time. The middle and distal segments of anterior descending branch of all rabbits were ligated to make AMI model. The level of aldosterone(Aldo) and the expression of endothelial nitric oxide synthase(eNOS) in coronary endotheliocyte which was located near the spot of deligation were determined 15 minutes postoperation. The hemodynamic state of left ventricular was measured and compared. Results: The eNOS expression of coronary endotheliocyte in both group A and B was weaker than that in group C, and that in group A was stronger than that in group B (P 〈 0.05 ). The level of Aldo in group A and B was much higher than that in group C ( P 〈 0.05 ), and there were no significant differences between group A and group B. The levels of mean systolic pressure ( MSP), mean diastolic pressure ( MDP), mean aterial blood pressure (MAP) and isovolumic contraction function( + dp/dt max) of left ventricular in group A and B were much higher than those in group C, and the changes of MSP and + dp/dt max of left ventricular in group A were more significant than those in group B. Conclusion: Spironolactone can enhance the expression of eNOS in coronary endotheliocyte that hasn't been deligated. Spironolactone could improve the hemodynamic state of heart in early period of AMI, and the possible mechanism might be connected with the fact that it can promote coronary dilation in non-infracted area in coordination with the non-genomic function of Aldo.
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