Cardiac arrest (CA) is a leading cause of mortality worldwide. Most of post-resuscitation related deaths are due to post-cardiac arrest syndrome (PCAS). After cardiopulmonary resuscitation (CPR), return of spontaneous circulation (ROSC) leads to renal ischemia-reperfusion injury, also known as PCAS. Many studies have focused on brain and heart injuries after ROSC, but renal failure has largely been ignored. Therefore, we investigated the protective effects of therapeutic hypothermia (TH) on asphyxial CA-induced renal injury in rats. Thirty rats were randomly divided into five groups: 1) the control group (sham); 2) the normothermic CA (nor.); 3) a normothermic CA group that received TH immediately within 2 h after CPR (Hypo. 2 hrs); 4) a normothermic CA group that received TH within 4 h after CPR (Hypo. 4 hrs); and 5) a normothermia CA group that received TH within 6 h after CPR (Hypo. 6 h). One day after CPR, all rats were sacrificed. Compared with the normothermic CA group, the TH groups demonstrated significantly increased survival rate (P < 0.05); decreased serum blood urea nitrogen, creatinine, and lactate dehydrogenase levels; and lower histological damage degree and malondialdehyde concentration in their renal tissue. Terminal deoxynucleotidyl transferase dUTP nick end labeling stain revealed that the number of apoptotic cells significantly decreased after 4 h and 6 h of TH compared to the results seen in the normothermic CA group. Moreover, TH downregulated the expression of cyclooxygenase-2 in the renal cortex compared to the normothermic CA group one day after CPR. These results suggest that TH exerts anti-apoptotic, anti-inflammatory, and anti-oxidative effects immediately after ROSC that protect against renal injury.

中文翻译：

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低温治疗对窒息性心脏骤停大鼠模型肾损伤的保护作用

心脏骤停 (CA) 是世界范围内导致死亡的主要原因。大多数与复苏后相关的死亡是由于心脏骤停后综合征 (PCAS)。心肺复苏 (CPR) 后，自主循环恢复 (ROSC) 导致肾缺血再灌注损伤，也称为 PCA。许多研究都集中在 ROSC 后的大脑和心脏损伤上，但肾功能衰竭在很大程度上被忽视了。因此，我们研究了治疗性低温 (TH) 对窒息性 CA 诱导的大鼠肾损伤的保护作用。30只大鼠随机分为五组：1）对照组（sham）；2）常温CA（nor.）；3）CPR后2小时内立即接受TH的常温CA组（Hypo.2hrs）；4）CPR后4小时内接受TH的常温CA组（Hypo.4hrs）；和5）CPR后6小时内接受TH的CA组常温（Hypo.6h）。CPR后一天，处死所有大鼠。与常温CA组相比，TH组存活率显着提高（P < 0.05）；血清尿素氮、肌酐和乳酸脱氢酶水平降低；降低其肾组织的组织学损伤程度和丙二醛浓度。末端脱氧核苷酸转移酶 dUTP 缺口末端标记染色显示，与常温 CA 组中观察到的结果相比，TH 4 小时和 6 小时后凋亡细胞的数量显着减少。此外，与CPR后1天的常温CA组相比，TH下调肾皮质中环氧合酶-2的表达。这些结果表明 TH 发挥具有抗凋亡、抗炎、