| 马 敏,赵智慧,张 媛,王丽斯,吕晓敏.七氟醚预处理介导AMPKα1通路对大鼠心肌缺血再灌注损伤的保护作用[J].,2022,(11):2042-2045 |
| 七氟醚预处理介导AMPKα1通路对大鼠心肌缺血再灌注损伤的保护作用 |
| Sevoflurane Preconditioning Mediates the Protective Effect of AMPKα1 Pathway on Myocardial Ischemia-reperfusion Injury in Rats |
| 投稿时间：2021-12-14 修订日期：2021-12-28 |
| DOI：10.13241/j.cnki.pmb.2022.11.007 |
| 中文关键词: 七氟醚 预处理 心肌缺血再灌注损伤 腺苷酸环化激酶α1 去甲肾上腺素的释放 心肌梗死 |
| 英文关键词: Sevoflurane Preconditioning Myocardial ischemia-reperfusion injury Adenylate cyclase α1 Norepinephrine release Myocardial infarction |
| 基金项目:内蒙古自治区自然科学基金项目（2019MS08091） |
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| 中文摘要: |
| 摘要 目的：探讨七氟醚预处理介导腺苷酸环化激酶（AMP-activated protein kinase，AMPK）α1通路对大鼠心肌缺血再灌注损伤（myocardial ischemia-reperfusion injury, MIRI）的保护作用。方法：将清洁级雄性SD大鼠60只随机平分为三组：模型组、地佐辛组与七氟醚组，三组均建立MIRI模型。地佐辛组与模型组都在建模前24 h腹腔注射地佐辛40 μg/kg与等剂量生理盐水，七氟醚组吸入2.5 %七氟醚15 min。结果：所有大鼠在建模过程中均存活，无大鼠因严重并发症而舍弃。地佐辛组与七氟醚组再灌注后24 h与48 h的左心室收缩压、左心室舒张末期压、心肌梗死面积百分比、血清去甲肾上腺素含量、心脏组织AMPKα1和皮质激素调节激酶-1（glucocorticoid-regulated kinase-1，GK1）蛋白相对表达水平都低于模型组（P<0.05），七氟醚组低于地佐辛组（P<0.05）。结论：七氟醚预处理可通过抑制大鼠MIRI的AMPKα1通路的激活和血清去甲肾上腺素释放，从而减少大鼠心肌梗死面积，并进一步促进心功能恢复正常。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the protective effect of sevoflurane preconditioning-mediated adenylate cyclic kinase (AMP-activated protein kinase, AMPK) α1 pathway on myocardial ischemia-reperfusion injury in rats. Methods: Sixty clean-grade male SD rats were randomly divided into three groups-model group, dezocine group and sevoflurane group. All three groups established myocardial ischemia-reperfusion injury models. Both the dezocine group and the model group were intraperitoneally injected with 40 μg/kg of dezocine and the same dose of normal saline 24 hours before modeling, and the sevoflurane group were inhaled with 2.5 % sevoflurane for 15 minutes. Results: All rats were survived in the modeling process, and there were no rats were abandoned due to severe complications. The LVSP, LVEDP, percentage of myocardial infarction area, serum norepinephrine content, cardiac tissue relative expression level of glucocorticoid-regulated kinase-1(GK1) and AMPKα1 protein at 24 h and 48 h after reperfusion in the dezocine group and sevoflurane group were lower than the model group(P<0.05), and the sevoflurane group were lower than the dezocine group(P<0.05). Conclusion: Sevoflurane pretreatment can reduce the myocardial infarct size in rats and further promote the return of normal cardiac function by inhibiting the activation of AMPKα1 pathway in MIRI and the release of serum norepinephrine in rats. |
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