Inhibition of mitochondrial reactive oxygen species improves coronary endothelial function after cardioplegic hypoxia/reoxygenation

The Journal of Thoracic and Cardiovascular Surgery

article

Yi Song¹  Hang Xing¹  Yixin He¹  Zhiqi Zhang¹  Guangbin Shi¹  Su Wu¹  Yuhong Liu¹  Elizabeth O. Harrington²  Frank W. Sellke¹  Jun Feng¹ 

[1] Division of Cardiothoracic Surgery, Rhode Island Hospital, Alpert Medical School of Brown University;Department of Medicine, Vascular Research Laboratory, Providence VA Medical Center, Alpert Medical School of Brown University

关键词: cardiac surgery;    cardioplegia;    cardioplegic arrest;    cardioplegic hypoxia and reoxygenation;    cardioplegic ischemia and reperfusion;    cardiopulmonary bypass;    coronary endothelial function;    coronary endothelium-dependent vasodilation;    coronary microcirculation;    diabetes;    endothelial function;    ion channels;    ischemia–reperfusion;    mitochondria;    mitochondrial reactive oxygen species;    potassium channels;    reactive oxygen species;    small conductance calcium-activated potassium channels;   

DOI  :  10.1016/j.jtcvs.2021.06.029

学科分类：心脏病和心血管学

来源: Mosby, Inc.

【 摘 要 】

Cardioplegic ischemia–reperfusion and diabetes mellitus are correlated with coronary endothelial dysfunction and inactivation of small conductance calcium-activated potassium channels. Increased reactive oxidative species, such as mitochondrial reactive oxidative species, may contribute to oxidative injury. Thus, we hypothesized that inhibition of mitochondrial reactive oxidative species may protect coronary small conductance calcium-activated potassium channels and endothelial function against cardioplegic ischemia–reperfusion-induced injury.

【 授权许可】

Unknown