山东大学学报 (医学版) ›› 2022, Vol. 60 ›› Issue (1): 1-5.doi: 10.6040/j.issn.1671-7554.0.2021.0275
• 基础医学 • 下一篇
黄辉宁1,2,杜娟娟2,孙燚2,侯应龙2,高梅1,2
HUANG Huining1,2, DU Juanjuan2, SUN Yi2, HOU Yinglong2, GAO Mei1,2
摘要: 目的 探讨硫化氢(H2S)减轻急性阻塞性睡眠呼吸暂停(OSA)诱发房颤的机制。 方法 硫氢化钠(NaHS)作为外源性H2S供体,8~10周龄健康成年雄性SD大鼠24只,体质量320~360 g,随机分为对照组、OSA诱发房颤组、NaHS+OSA组和氯化镉+NaHS+OSA组,每组6只。按照既往文献构建OSA诱发房颤模型,实验结束后处死大鼠,留取左心耳组织。采用免疫荧光、ELISA法检测左心耳谷氧还蛋白-1的表达水平;采用硫代巴比妥酸法检测左心耳丙二醛(MDA)含量。 结果 与OSA组相比,NaHS+OSA组房颤诱发次数减少、房颤持续时间缩短(P<0.05);与对照组相比,OSA组左心耳谷氧还蛋白-1表达减少,MDA含量增加,应用NaHS后,NaHS+OSA组谷氧还蛋白-1表达水平较OSA组增加,MDA含量降低(P<0.01),在NaHS基础上应用谷氧还蛋白-1抑制剂氯化镉后,氯化镉+NaHS+OSA组MDA含量增加(P<0.01),H2S减轻OSA诱发房颤的作用消失。 结论 外源性H2S减轻急性OSA诱发房颤,可能是通过上调心肌细胞谷氧还蛋白-1表达从而减轻心肌细胞氧化应激。
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