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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。
OBJECTIVE: To investigate the effect of co-expression of AAV-PR39-ADM on angiotensin-converting enzyme (PR39) and vasodilator peptide (ADM) on myocardial ischemia-reperfusion injury in SD rats. Methods: Thirty-six healthy adult male Sprague-Dawley rats weighing 280 g ± 20 g were randomly divided into sham operation group (SO), treatment group (TR) and control group (I / R) . The myocardium of the treated group was injected with AAV-PR39-ADM into the myocardium for 7 days. The left ventricular wall thickness and ejection fraction (EF%), left ventricular end-systolic pressure (LVSP) and left ventricular pressure Rise and descent rates (± dp / dt max) were evaluated as cardiac function indicators. In the control group, a model of ischemia-reperfusion injury was established. In the sham operation group, only the thread was not ligated and the same test was performed in both groups. The rats were sacrificed and their myocardial infarction area was measured by Masson staining. Results: The treatment group was significantly higher than that of the control group. The ejection fraction, left ventricular end-systolic pressure, maximum rate of ascending, maximum rate of decrease and infarct size were respectively 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, 107), (1886 ± 124), P <0.05; IS% :( 29.3 ± 4.6), (24.6 ± 2.2), P <0.05. Conclusion: AAV-PR39-ADM can significantly reduce the left ventricular pressure drop caused by myocardial ischemic injury, improve myocardial contractility, improve ejection fraction and significantly reduce the range of myocardial infarction.