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作 者:赵茹[1] 张茹艳[2] 宋衍秋[3] 胡越成[1] 丛洪良[1]
机构地区:[1]天津市胸科医院心内科,天津300051 [2]天津医科大学临床学院 [3]天津市心血管病研究所
出 处:《临床心血管病杂志》2013年第7期549-550,共2页Journal of Clinical Cardiology
摘 要:急性心肌梗死(AMI)后心脏利钠肽系统即被激活,导致心室B型钠尿肽(BNP)水平升高,一方面,可对抗肾素-血管紧张素-醛固酮系统(RAAS)的缩血管作用,另一方面,压力及容量负荷促进心肌组织分泌心房钠尿肽和BNP的同时,Summary We observed the changes of TNF-α and BNP in rats after acute myocardial infarction (AMI), and examined the effect of Cilazapril on them. Seventy Wistar male rats were randomly divided into sham-operated group and operated group, the latter was further divided into AMI group and Cilazapril group. There were signifi- cant differences between AM1 group and sham-operated group concerning the levels of TNF-α and BNP in plasma. TNFα and BNP in Cilazapril group were significantly lower comparing with AMI group. Cilazapril can reduce TNF-α and BNP in blood and myocardial.
关 键 词:心肌梗死 急性 西拉普利 B型利钠肽 肿瘤坏死因子-Α
分 类 号:R542.2[医药卫生—心血管疾病]
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