Department of Emergency Medicine National Taiwan University Medical College and Hospital Taipei Taiwan.
Medical Intensive Care Unit Cathay General Hospital Taipei Taiwan.
J Am Heart Assoc. 2021 May 18;10(10):e019837. doi: 10.1161/JAHA.120.019837. Epub 2021 May 7.
Background Steroid use after cardiac arrest has been reported to improve survival and neurological outcome in cardiac arrest survivors. The study aimed to evaluate the effect of post-arrest hydrocortisone use on myocardial damage and cardiac mitochondrial injury in a rat model of ventricular fibrillation cardiac arrest. Methods and Results Ventricular fibrillation cardiac arrest was induced and left untreated for 5 minutes in adult male Wistar rats. Cardiopulmonary resuscitation and electric shocks were then applied to achieve return of spontaneous circulation (ROSC). Successfully resuscitated animals were randomized into 3 groups: control, low-dose hydrocortisone (2 mg/kg), and high-dose hydrocortisone (8 mg/kg). The low-dose hydrocortisone and high-dose hydrocortisone (treatment) groups received intravenous hydrocortisone immediately after ROSC and the control group received saline as placebo. Each group consisted of 15 animals. Within 4 hours of ROSC, both treatment groups showed a higher cardiac output than the control group. At the fourth hour following ROSC, histological examination and transmission electron microscopy demonstrated less myocardial damage and mitochondrial injury in the animals treated with hydrocortisone. In the treatment groups, hydrocortisone mitigated the acceleration of Ca-induced mitochondrial swelling and suppression of complex activity observed in the control group. At the 72nd hour after ROSC, a significantly higher proportion of animals treated with hydrocortisone survived and had good neurological recovery compared with those given a placebo. Conclusions Hydrocortisone use after cardiac arrest may mitigate myocardial injury and cardiac mitochondrial damage and thus improve survival, neurological and histological outcomes in a rat model of ventricular fibrillation cardiac arrest.
有报道称，心脏骤停后使用类固醇可提高心脏骤停幸存者的存活率和神经功能预后。本研究旨在评估心脏停搏后使用氢化可的松对心室颤动性心脏骤停大鼠模型心肌损伤和心脏线粒体损伤的影响。
成年雄性 Wistar 大鼠诱导心室颤动性心脏骤停，不进行治疗 5 分钟。然后进行心肺复苏和电击以实现自主循环恢复（ROSC）。成功复苏的动物随机分为 3 组：对照组、低剂量氢化可的松（2mg/kg）组和高剂量氢化可的松（8mg/kg）组。低剂量氢化可的松和高剂量氢化可的松（治疗）组在 ROSC 后立即给予静脉内氢化可的松，对照组给予生理盐水作为安慰剂。每组包含 15 只动物。在 ROSC 后 4 小时内，两组治疗组的心输出量均高于对照组。在 ROSC 后第 4 小时，组织学检查和透射电镜显示，氢化可的松治疗组的心肌损伤和线粒体损伤较轻。在治疗组中，氢化可的松减轻了对照组中观察到的 Ca 诱导的线粒体肿胀加速和复合物活性抑制。在 ROSC 后 72 小时，与给予安慰剂的动物相比，接受氢化可的松治疗的动物的存活率明显更高，且神经功能恢复良好。
心脏骤停后使用氢化可的松可能减轻心肌损伤和心脏线粒体损伤，从而改善心室颤动性心脏骤停大鼠模型的存活率、神经和组织学结局。
