Patients undergoing cardiopulmonary bypass (CPB) often develop acute kidney injury (AKI) caused by myocardial ischemia reperfusion (MI/R), and this renal injury can be resolved notably by dexmedetomidine. Endoplasmic reticulum (ER) stress was reported to get involved in organ injury including AKI. The current study aimed to address the correlation between MI/R induced AKI with ER stress and to assess the effects of dexmedetomidine pretreatment on AKI protection. Patients selected for heart valve replacement surgery were randomly assigned to NS group (pre-anesthesia with 0.9% NaCl) and DEX group (pre-anesthesia with dexmedetomidine). Rat MI/R model was induced by occluding coronary artery for 30 min followed by 48-hour reperfusion. Rats were randomized into Sham (0.9% NaCl), I/R (MI/R + 0.9% NaCl) and I/R + DEX (MI/R + dexmedetomidine). Organ function and ER stress condition were evaluated by blood chemistry, pathology, and molecular test. Clinical data indicated dexmedetomidine pretreatment attenuated AKI and oxidative stress as well as postischemic myocardial injury in patients. Accordingly animal results suggested dexmedetomidine reduced cellular injury and improved postischemic myocardial and renal function. Dexmedetomidine also reduced myocardial and renal cells apoptosis and down-regulated ER stress. These results suggested that dexmedetomidine pretreatment attenuates MI/R injury-induced AKI by relieving the ER stress.

中文翻译：

---

右美托咪定预处理可减轻人和大鼠心肌缺血再灌注引起的急性肾损伤和内质网应激

接受体外循环（CPB）的患者经常会出现由心肌缺血再灌注（MI/R）引起的急性肾损伤（AKI），而右美托咪定可以显着缓解这种肾损伤。据报道，内质网 (ER) 应激与器官损伤（包括 AKI）有关。本研究旨在探讨 MI/R 诱发的 AKI 与 ER 应激之间的相关性，并评估右美托咪定预处理对 AKI 保护的效果。选择接受心脏瓣膜置换手术的患者被随机分为 NS 组（预麻醉用 0.9% NaCl）和 DEX 组（预麻醉用右美托咪定）。通过闭塞冠状动脉30分钟然后再灌注48小时来诱导大鼠MI/R模型。大鼠被随机分为 Sham (0.9% NaCl)、I/R (MI/R + 0.9% NaCl) 和 I/R + DEX (MI/R + 右美托咪定)。通过血液化学、病理学和分子检测评估器官功能和内质网应激状况。临床数据表明，右美托咪定预处理可减轻患者的 AKI 和氧化应激以及缺血后心肌损伤。因此，动物结果表明右美托咪定减少了细胞损伤并改善了缺血后心肌和肾功能。右美托咪定还可以减少心肌和肾细胞凋亡并下调内质网应激。这些结果表明，右美托咪定预处理可通过缓解 ER 应激来减轻 MI/R 损伤诱发的 AKI。