INTRACORONARY ADENOSINE ADMINISTRATION DURING REPERFUSION FOLLOWING 3 HOURS OF ISCHEMIA - EFFECTS ON INFARCT SIZE, VENTRICULAR-FUNCTION, AND REGIONAL MYOCARDIAL BLOOD-FLOW
INTRACORONARY ADENOSINE ADMINISTRATION DURING REPERFUSION FOLLOWING 3 HOURS OF ISCHEMIA - EFFECTS ON INFARCT SIZE, VENTRICULAR-FUNCTION, AND REGIONAL MYOCARDIAL BLOOD-FLOW
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DOI：
10.1016/0002-8703(90)90196-5
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发表时间：
1990-10-01
影响因子：
4.8
通讯作者：
FORMAN, MB
中科院分区：
文献类型：
--
作者：
BABBITT, DG;VIRMANI, R;FORMAN, MB
先前的研究表明，腺苷显著增强局部缺血90分钟后的心肌挽救。为了确定其在长时间缺血后的作用，闭胸犬进行了3小时的左前降支动脉闭塞，然后再灌注72小时。在再灌注的前60分钟内，将冠状动脉内腺苷（3.75 mg/min;以1.5 ml/min：总体积= 90 ml; n = 10）或等量生理盐水（1.5 ml/min：总体积= 90 ml; n = 9）输注到左冠状动脉主干中。用微球连续评价局部心肌血流量，用对比心室造影评价局部心室功能。组织学上确定肿瘤大小。光镜和电镜观察中性粒细胞浸润和微血管损伤。腺苷不能减少梗死面积，以危险面积的百分比表示（38.0 ± 0.1%）。4.9%对34.8 .+-. 4.6%; p = NS）或改善局部心室功能（3.2 . ±. 1.8%对2.2 .+-。3.1%; p = NS）。在腺苷给药期间，在缺血区的心肌内膜和中层区域未观察到血管舒张作用。这与腺苷处理组和生理盐水对照组中相似程度的毛细血管内皮变化和中性粒细胞浸润相关。这些结果表明，严重的功能异常存在于血管缺血3小时后，腺苷治疗是无效的，在提高心肌挽救。
Previous studies have demonstrated that adenosine significantly enhances myocardial salvage after 90 minutes of regional ischemia. To determine its effect after prolonged ischemia, closed-chest dogs underwent 3 hours of left anterior descending artery occlusion followed by 72 hours of reperfusion. Intracoronary adenosine (3.75 mg/min; at 1.5 ml/min:total volume = 90 ml; n = 10) or an equivalent volume of saline (1.5 ml/min: total volume = 90 ml; n = 9) was infused into the left main coronary artery during the first 60 minutes of reperfusion. Regional myocardial blood flow was assessed serially with microspheres and regional ventricular function was assessed by contrast ventriculography. Infarct size was determined histologically. Light and electron microscopy were utilized to assess neutrophil infiltration and microvascular injury. Adenosine failed to reduce infarct size expressed as a percentage of the area at risk (38.0 .+-. 4.9% versus 34.8 .+-. 4.6%; p = NS) or to improve regional ventricular function as measured by the radial shortening method (3.2 .+-. 1.8% versus 2.2 .+-. 3.1%; p = NS) at 72 hours after reperfusion. Vasodilatory effects were not observed in the endo- and midmyocardial regions of the ischemic zone during adenosine administration. This was associated with a similar extent of capillary endothelial changes and neutrophil infiltration in both adenosine-treated and saline control groups. These results suggest that severe functional abnormalities are present in the vasculature after 3 hours of ischemia and that adenosine therapy is ineffective in enhancing myocardial salvage.