Background Myocardial ischemia-reperfusion injury (MIRI) has been confirmed to induce endoplasmic reticulum stress(ERS) during downstream cascade reaction when myocardial cell function keep deteriorating to a certain degree. The fact of matter is the clinical inconsistence with experimental outcomes still exist due to the mechanism has not been entirely clarified. Dexmedetomidine (DEX), a new generation anti-inflammatory and organ protector, has been testified can attenuate the IRI of heart. This study aimed to find out if DEX had the capacity to protect the injured cardiomyocytes under in vitro hypoxia/reoxygenation circumstance and if the ERS was totally or partly intervened.

中文翻译：

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右美托咪定部分通过抑制内质网应激来减轻缺氧/复氧条件下对H9C2心肌的损伤

背景技术心肌缺血再灌注损伤（MIRI）在心肌细胞功能持续恶化至一定程度的下游级联反应中，可诱导内质网应激（ERS）。事实是，由于机理尚未完全阐明，临床仍与实验结果不一致。新一代抗炎和器官保护剂右美托咪定（DEX）已被证明可以减弱心脏的IRI。这项研究旨在发现DEX是否有能力在体外缺氧/复氧的情况下保护受损的心肌细胞，以及是否完全或部分干预了ERS。