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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].现代生物医学进展英文版,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）

Author Name	Affiliation
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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