七氟醚介导的氧化性心肌损伤的调节

IF 1.2 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Siavash Sedghi, Wiam Z. Khadra, Leili Pourafkari, Paul R. Knight, Faraz A. Alderson, Nader D. Nader
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引用次数: 0

摘要

简介:挥发性麻醉剂在整个缺血性损伤过程中提供保护。我们研究了挥发性麻醉剂如何调节与过氧化氢相关的心肌细胞损伤。方法:48只Long-Evans大鼠根据治疗方法分为4组:无治疗组(CONT)、格列本脲组(GLB);七氟醚(签订);或GLB +塞。每组进一步分成两组,其中一组暴露于过氧化氢(H2 O2)。心肌分离前48小时口服GLB。所有大鼠均腹腔注射氯胺酮麻醉,肝素化后摘取心脏。心肌细胞分离使用机械切碎和酶消化的组合。分离后,将细胞等分暴露于h2o2和FeSO4中30分钟。然后用100%氧气和1.5% SEV(如果合适)使细胞悬液起泡10分钟。采用荧光素结合膜联蛋白- v检测各组细胞凋亡,碘化丙啶检测坏死,ELISA检测各组caspase-3活性。结果:过氧化氢暴露后,细胞凋亡、坏死和caspase-3活性增加。SEV可降低细胞坏死和凋亡率。GLB预处理不改变SEV的效果。同样,caspase-3活性也不随GLB而改变,尽管SEV处理在过氧化氢反应中降低了这种酶的活性。结论:在这个氧化损伤模型中,我们证明了与SEV孵育分离的心肌细胞相比,H2 O2诱导的凋亡和坏死细胞明显减少。这些结果支持了KATP通道不是与麻醉预处理相关的唯一介质的假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sevoflurane-mediated modulation of oxidative myocardial injury
Introduction: Volatile anesthetics offer protection when administered throughout an ischemic injury. We examined how volatile anesthetics modulate the cardiac myocytic injury associated with hydrogen peroxide. Methods: Forty-eight Long-Evans rats were divided into four groups depending on the treatment: none (CONT), Glibenclamide (GLB); Sevoflurane (SEV); or GLB+SEV. Each group was further divided into two, one of which was exposed to hydrogen peroxide (H2 O2 ). Oral GLB was administered 48 hours before myocardial isolation. All rats were anesthetized by intraperitoneal injection of Ketamine, and the hearts were harvested after heparinization. Cardiomyocytes were isolated using a combination of mechanical mincing and enzymatic digestion. After isolation, the aliquots of cells were exposed to H2 O2 and FeSO4 for 30 minutes. The cell suspensions were then bubbled for 10 minutes with 100% oxygen and 1.5% SEV if appropriate. Apoptosis was detected by fluorescein-bound annexin-V (ANX-V), necrosis by propidium iodide, and ELISA assessed caspase-3 activity in all groups. Results: There was an increase in apoptosis, necrosis, and caspase-3 activity in the cells following exposure to hydrogen peroxide. SEV reduced the rate of cell necrosis and apoptosis. Pretreatment with GLB did not alter the effects of SEV. Similarly, caspase-3 activity did not change with GLB, although SEV administration reduced this enzymatic activity in response to hydrogen peroxide. Conclusion: In this oxidant injury model, we demonstrated that incubating isolated cardiomyocytes with SEV profoundly diminished H2 O2 -induced apoptotic and necrotic cells compared to their CONTs. These results support the hypothesis that KATP channels are not the sole mediators associated with anesthetic preconditioning.
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来源期刊
Journal of Cardiovascular and Thoracic Research
Journal of Cardiovascular and Thoracic Research CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
2.00
自引率
0.00%
发文量
22
审稿时长
7 weeks
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