由内皮衍生的氧化通过调节线粒体电子运输的过程来调节后血性心肌氧化和氧气消耗
Xue Zhao1, Guanglong He, Yeong-Renn Chen
1Center for Biomedical EPR Spectroscopy and Imaging, the Davis Heart and Lung Research Institute, and the Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, Ohio, USA.
源自内皮氧化合成酶 (eNOS) 的氧化 (NO) 抑制了心脏缺血后的氧气消耗. 这种对线粒体呼吸的调节会影响心肌重塑.
科学领域:
- 心血管生理学心血管生理学
- 线粒体呼吸 线粒体呼吸
- 缺血性心脏病是一种心脏病.
背景情况:
- 氧化 (NO) 水平在心脏组织中升高.
- 已知NO在体外调节线粒体的氧气消耗.
- 内皮NO合成酶 (eNOS) 衍生的NO在心脏缺血后氧气消耗中的体内作用需要研究.
研究的目的:
- 在实体中研究eNOS衍生的NO在调节心脏缺血后的氧气消耗中的作用.
- 为了确定NO如何影响线粒体呼吸和心肌氧张力在再注射期间.
主要方法:
- 小鼠经历了冠状动脉绑定,然后再输血.
- 心肌中氧气张力 (Po2) 用电子偏磁共振氧度法测量.
- 实验涉及野生类型,N-nitro-L-arginine甲基 (L-NAME) 处理和eNOS淘汰 (eNOS-/-) 的小鼠.
主要成果:
- 与野生型小鼠相比,L-NAME治疗和eNOS-/-治疗小鼠的心肌PO2在再输血后显著降低.
- eNOS衍生的NO降低了速率-压力产物,并抑制了NADH脱酶 (NADH-DH) 的活性.
- NO上调细胞染色体c氧化酶 (CcO) mRNA表达和增加过氧酸盐的形成.
结论:
- eNOS衍生的NO显著抑制后缺血性心脏中的氧气消耗.
- NO通过改变NADH-DH和CcO酶活性和mRNA表达来调节线粒体呼吸.
- 在NO的影响下,心肌氧张力增加后的再输液,可能会触发后缺血性重塑.
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