Veno-arterial extracorporeal membrane oxygenation reduces myocardial and mitochondrial damage in acute myocardial infarction

体外膜肺氧合 心肌梗塞 心脏病学 医学 内科学 充氧
作者
Ming Ni,Aiqiang Dong,Xian Zhu,Xuebiao Li,Guocong Xu,Ning Gao,Dongdong Wei,Yifan Wang,Minjian Kong
出处
期刊:Shock [Ovid Technologies (Wolters Kluwer)]
卷期号:62 (1): 111-118
标识
DOI:10.1097/shk.0000000000002361
摘要

ABSTRACT Background: Myocardial infarction (MI) is a common cardiovascular disease with a high fatality rate once accompanied by cardiogenic shock. The efficacy of extracorporeal membrane oxygenation (ECMO) in treating MI is controversial. Methods: MI was induced by ligating the left anterior descending artery (LAD) in adult male rats. Groups were defined as follows: MI group, reperfusion for 90 min after 30 min of LAD occlusion; MI + ECMO group, reperfusion and ECMO were performed for 90 min immediately after 30 min of LAD occlusion; prolonged MI + ECMO group, ECMO was used immediately after 30 min of occlusion with persistent occlusion of the LAD for an additional 30 min, followed by 90 min of reperfusion. The myocardial infarct size and mitochondrial morphology and function data were collected and compared of each group. Results: The ECMO groups had a smaller myocardial infarct size and larger percentage ejection fraction. Compared with the prolonged MI + ECMO group, the immediate reperfusion group had a lower percentage of infarct size (63.28% vs. 17.97% vs. 31.22%, MI vs. MI + ECMO vs. prolonged MI + ECMO). Mitochondria isolated from the ischemic zone showed an intact mitochondrial structure, including fewer voids and broken cristae, and preserved activity of mitochondrial complex II and complex IV in ECMO groups. Conclusions: ECMO support in MI can reduce myocardial injury despite delayed coronary reperfusion.

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