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首页> 外文期刊>Molecular biology reports >The changes of technetium-99m-labeled annexin-V in delayed anesthetic preconditioning during myocardial ischemia/reperfusion
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The changes of technetium-99m-labeled annexin-V in delayed anesthetic preconditioning during myocardial ischemia/reperfusion

机译:m-99m标记的膜联蛋白V在心肌缺血/再灌注期间延迟麻醉预适应中的变化

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This study was designed to use real-time imaging to test the hypothesis that delayed cardiac protection induced by volatile anesthetics inhibits apoptosis. Rats were divided into two groups. One group was exposed to 120 min of 33 % O-2 [control group (CON group)] and the other group was exposed to 2.5 % sevoflurane in 33 % O-2 for 120 min [sevoflurane group (SEVO group)]. Both groups were allowed to return to their cages for 24 h. After 24 h recovery, all rats underwent 30 min myocardial ischemia by occluding coronary artery followed by 2 h of reperfusion. After reperfusion, technetium-99m-labeled annexin-V was administered intravenously to identify apoptosis. Left ventricular samples were obtained to measure infarct size and radionuclide imaging and caspase-3. Radionuclide imaging indicated that apoptosis was reduced in SEVO group (0.78 % +/- A 0.82) when compared with the CON group (1.15 % +/- A 0.61), and the infarct size was also decreased in the SEVO group (40 % +/- A 7). The transferase dUTP nick end labeling (TUNEL)-positive cardiomyocytes in the SEVO group (16 % +/- A 6) were significantly decreased in the peri-infarct zone when compared with the CON group (28 % +/- A 4). After reperfusion, caspase-3 expression was significantly blunted in the SEVO group than in CON group (50 % +/- A 11 vs. 68 % +/- A 10, p < 0.05). This study used technetium-99m-labeled annexin-V of real-time imaging to detect cardiomyocyte apoptosis and the results were confirmed by the TUNEL assay and caspase-3 expression. We concluded that delayed volatile anesthetic preconditioning (APC) protects against I/R in vivo. The method of technetium-99m-labeled annexin-V of real-time imaging can be used to detect cardiomyocyte apoptosis in delayed APC during ischemia/reperfusion.
机译:本研究旨在使用实时成像来检验以下假设:挥发性麻醉药诱导的延迟心脏保护作用会抑制细胞凋亡。将大鼠分为两组。一组暴露于33%O-2的120分钟[对照组(CON组)],另一组暴露于33%O-2中的2.5%七氟醚120分钟[七氟醚组(SEVO组)]。两组均被允许返回其笼子24小时。恢复24小时后,所有大鼠均通过阻塞冠状动脉进行30分钟的心肌缺血,然后再灌注2 h。再灌注后,静脉内注射tech 99m标记的膜联蛋白V以鉴定细胞凋亡。获得左心室样品以测量梗塞大小,放射性核素成像和caspase-3。放射性核素显像表明SEVO组的细胞凋亡减少了(0.78%%+/- A 0.82),而CON组的细胞凋亡减少了(1.15%%+/- A 0.61),SEVO组的梗死面积也减少了(40%+ /-A 7)。与CON组相比(28%+/- A 4),SEVO组中的转移酶dUTP缺口末端标记(TUNEL)阳性心肌细胞(16%+/- A 6)在梗死灶周围区域显着减少。再灌注后,SEVO组的caspase-3表达明显低于CON组(50%+/- A 11对68%+/- A 10,p <0.05)。这项研究使用tech 99m标记的膜联蛋白V实时成像检测心肌细胞凋亡,并通过TUNEL分析和caspase-3表达证实了该结果。我们得出的结论是,延迟性挥发性麻醉剂预处理(APC)在体内可预防I / R。 m- 99m标记的膜联蛋白-V实时成像方法可用于检测缺血/再灌注期间延迟APC中的心肌细胞凋亡。

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