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心肌缺血与脑钠素分泌机制研究

Secretion of brain natriuretic peptide and myocardial ischemia
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摘要 目的:了解心肌缺血是否是引起脑钠素(BNP)的分泌原因。方法:(1)建立反复3 min缺血3次再灌注5 min心肌缺血模型。(2)用电生理记录仪动态观察缺血再灌注前后心脏功能(LVSP、LVEDP)和心电图的改变。(3)用ELISA法测定血浆中BNP值。结果:(1)心肌缺血组和对照组LVSP、LVEDP在整个实验过程中无明显改变。(2)心肌经反复3次3 min缺血5 min再灌注后BNP分泌增加,再灌注15 min时,心肌缺血组BNP值升至最高[(240.14±21.55)pg/ml],再灌注45 min时心肌缺血组BNP值恢复至基线水平;对照组BNP值在整个实验过程中无明显改变。(3)缺血组在心肌缺血后心电图ST段逐渐抬高,再灌注后ST段逐渐回落,再灌注15 min左右回到基线,实验过程中心率无增快;对照组心电图在整个实验过程中未发生改变。结论:心肌缺血是引起脑钠素分泌的一种机制。 ObjectiveTo understand whether secretion of brain natriuretic peptide(BNP)is caused bymyocardial ischemia or not.Method①The experimental model of myocardial ischemia was developed.②To record LVSP、LVEDP and ECG by electrophysiological recorder before and after ischemic reperfusion.③Value of BNP was measured by ELISA method.Results①LVSP and LVEDP of control group andmyocardial ischemia group was not affected.②Value of BNP of myocardial ischemiagroup gradually rises,was at the highest[(240.14±21.55)pg/ml]on 15 minpointafter reperfusion,was completely recovered on 45 min point after reperfusion.Value of BNP of control group was not affected.③ST segment in ECG of myocardial ischemia group gradually rises,falls after reperfusion,was completely recovered on15 min point after reperfusion.Conclusion Myocardial ischemia could lead to secretion of BNP.
出处 《吉林医学》 CAS 2018年第4期605-607,共3页 Jilin Medical Journal
基金 四川省卫计委资助课题[项目编号:080023]
关键词 心肌缺血 脑钠素 分泌机制 Myocardial ischemia BNP Secretory m echanism
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