文章摘要
李海勋 席聪 安睿 申国宏 李聪叶 王跃民 孙立军.共载体AAV-PR39-ADM 治疗缺血性心脏病[J].,2015,15(13):2401-2404
共载体AAV-PR39-ADM 治疗缺血性心脏病
Co-integrated Vector of AAV-PR39-ADMTherapy Ischemic Heart Disease
  
DOI:
中文关键词: 血管生成肽(PR39)  血管扩张肽(ADM)  心肌缺血再灌注  基因治疗
英文关键词: Proline-arginine-rich peptide (PR39)  Adrenomedullin(ADM)  Ischemia Reperfusion  Gene Therapy
基金项目:国家自然科学基金项目(81170185)
作者单位
李海勋 席聪 安睿 申国宏 李聪叶 王跃民 孙立军 第四军医大学西京医院放射科全军医学影像中心宝鸡市人民医院神经内科 武警山西省总队医院综合科第四军医大学西京医院心血管内科全军心血管病研究所第四军医大学基础部生理学教研室陕 
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中文摘要:
      目的:探讨共载体AAV-PR39-ADM 分泌表达血管生成肽(PR39)与血管扩张肽(ADM)对SD大鼠心肌缺血再灌注损伤的作 用。方法:选健康成年雄性SD 大鼠36 只,体重平均为280 g± 20 g,随机分为假手术组(SO)、治疗组(TR)与对照组(I/R),每组各12 只。治疗组大鼠心肌注射共载体AAV-PR39-ADM 感染心肌7 天后行B超检查,测量记录左室壁厚度及射血分数(EF%),左室收 缩末压(LVSP),左室内压最大上升下降速率(± dp/dt max)评价作为心脏功能指标。对照组建立缺血再灌注损伤模型,假手术组只 穿线不结扎且两组行相同检测。速取处死大鼠心肌行masson 染色测量心肌梗死面积。结果:治疗组明显高于对照组,其射血分 数、左室内收缩末压、最大上升速率,最大下降速率、梗死面积分别为:EF%(50.4± 6.3),(29.8± 10.5),P<0.05;LVSP:(116± 4.2), (101± 3.7),P<0.05;+dp/dt max:(2859± 365),(2137± 191),P<0.05;-dp/dtmax:(2186± 107),(1886± 124),P<0.05; IS%:(29.3± 4.6), (24.6± 2.2),P<0.05。结论:共载体AAV-PR39-ADM能够显著恢复心肌缺血损伤引起的左室内压下降,提高心肌收缩能力,提高射 血分数并明显缩小心肌梗死范围。
英文摘要:
      Objective:To discuss the curative effect of the co-integrated vector of AAV-PR39-ADM which secret angiogenesis peptide (PR39) and Adrenomedullin(ADM) on a rat ischemia-reperfusion injury model.Methods:36 healthy adult male SD rats, weight 280g± 20g were randomly divided into sham-operation(SO), the treatment group (TR) and control group (I/R) each12. Ischemia-reperfusion injury model was established in both TR group and I/R group and co-integrated vector of AAV-PR39-ADMwas injected into the injured myocardiumof the treatment group rats. Echocardiographic measurement and record left ventricular systolic pressure (LVSP), maximal rate of rise of ventricular pressure (+dp/dt max), maximal rate of decline of ventricular pressure (-dp/dt max) and ejection fraction (EF %) were the treatment group rat of co-integrated vector of AAV-PR39-ADM transshipment myocardium after 7 days. The sham group was operated without coronary artery ligation. Hearts were speedy extracted after the execution of the rats, MASSON staining was carried out in the experiment.Results:The ejection fraction, left ventricular systolic pressure, maximum rate of left ventricular pressure rise or fall of the treatment group were significantly higher than those in control group [EF%(50.4± 6.3), (29.8± 10.5), P<0.05; LVSP: (116± 4.2), (101± 3.7), P<0.05; +dp/dt max: (2859± 365), (2137± 191), P<0.05; -dp/dtmax: (2186± 107), (1886± 124), P<0.05; IS%: (29.3± 4.6), (24.6± 2.2), P<0.05.].Conclusion:Co-integrated vector of AAV-PR39-ADMsignificantly attenuated the declines of LVSP, increased the myocardial contraction ability, improved the ejection fraction and obviously reduced infarct size.
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