Wang Changsheng, Bischof Evelyne, Xu Jing, Guo Qinyue, Zheng Guanghui, Ge Weiwei, Hu Juntao, Georgescu Margarint Elena Laura, Bradley Jennifer L, Peberdy Mary Ann, Ornato Joseph P, Zhu Changqing, Tang Wanchun
Department of Emergency Medicine, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Weil Institute of Emergency and Critical Care Research, Virginia Commonwealth University, Richmond, VA, United States.
Front Cardiovasc Med. 2022 Jul 7;9:894004. doi: 10.3389/fcvm.2022.894004. eCollection 2022.
Previous studies have demonstrated that inflammation and impaired microcirculation are key factors in post-resuscitation syndromes. Here, we investigated whether methylprednisolone (MP) could improve myocardial function and microcirculation by suppressing the systemic inflammatory response following cardiopulmonary resuscitation (CPR) in a rat model of cardiac arrest (CA).
Sprague-Dawley rats were randomly assigned to (1) sham, (2) control, and (3) drug groups. Ventricular fibrillation was induced and then followed by CPR. The rats were infused with either MP or vehicle at the start of CPR. Myocardial function and microcirculation were assessed at baseline and after the restoration of spontaneous circulation. Blood samples were drawn at baseline and 60-min post-resuscitation to assess serum cytokine (TNF-α, IL-1β, and IL-6) levels.
Myocardial function [estimated by the ejection fraction (EF), myocardial performance index (MPI), and cardiac output (CO)] improved post-ROSC in the MP group compared with those in the control group ( < 0.05). MP decreased the levels of the aforementioned pro-inflammatory cytokines and alleviated cerebral, sublingual, and intestinal microcirculation compared with the control ( < 0.05). A negative correlation emerged between the cytokine profile and microcirculatory blood flow.
MP treatment reduced post-resuscitation myocardial dysfunction, inhibited pro-inflammatory cytokines, and improved microcirculation in the initial recovery phase in a CA and resuscitation animal model. Therefore, MP could be a potential clinical target for CA patients in the early phase after CPR to alleviate myocardial dysfunction and improve prognosis.
先前的研究表明，炎症和微循环受损是复苏后综合征的关键因素。在此，我们研究了甲基强的松龙（MP）是否能通过抑制心脏骤停（CA）大鼠模型心肺复苏（CPR）后的全身炎症反应来改善心肌功能和微循环。
将Sprague-Dawley大鼠随机分为（1）假手术组、（2）对照组和（3）药物组。诱发室颤，然后进行心肺复苏。在心肺复苏开始时给大鼠输注MP或赋形剂。在基线和自主循环恢复后评估心肌功能和微循环。在基线和复苏后60分钟采集血样，以评估血清细胞因子（TNF-α、IL-1β和IL-6）水平。
与对照组相比，MP组自主循环恢复后心肌功能[通过射血分数（EF）、心肌性能指数（MPI）和心输出量（CO）评估]有所改善（<0.05）。与对照组相比，MP降低了上述促炎细胞因子的水平，并改善了脑、舌下和肠道的微循环（<0.05）。细胞因子谱与微循环血流量之间呈负相关。
在CA和复苏动物模型中，MP治疗减轻了复苏后心肌功能障碍，抑制了促炎细胞因子，并改善了初始恢复阶段的微循环。因此，MP可能是CA患者心肺复苏后早期减轻心肌功能障碍和改善预后的潜在临床靶点。
