Cho Young-Duck, Park Sung-Jun, Choi Sung-Hyuk, Yoon Young-Hoon, Kim Jung-Youn, Lee Sung-Woo, Lim Chae-Seung
Department of Emergency Medicine, Korea University College of Medicine, Seoul, Korea.
The institute for Trauma Research, Korea University, Seoul, Korea.
Ann Surg Treat Res. 2017 Oct;93(4):217-224. doi: 10.4174/astr.2017.93.4.217. Epub 2017 Sep 28.
Postcardiac arrest syndrome (PCAS) shares many features with sepsis including plasma cytokine elevation with dysregulation of cytokine production, and the presence of endotoxin in plasma. PCAS is closely related to ischemia-reperfusion injury. During ischemia-reperfusion injury, neutrophil, which is the first line of innate immunity, plays a major role. In this study, we investigated the inflammatory response of human neutrophils in an model which we simulated with hypoxia-normoxia and hypoxia-hyperoxia environments.
After separation of neutrophils from the whole blood, they were divided into 3 experimental groups: normoxia-normoxia, hypoxia-normoxia, and hypoxia-hyperoxia groups. The production of HO, the expression of Toll-like receptor 4 (TLR) receptor, and the extent of apoptosis of the neutrophils were checked.
The hypoxia-normoxia and -hyperoxia models, which simulated the PCAS, showed initiation of the neutrophils' inflammatory reaction by hypoxia insult. Lipopolysaccharide amplifies such inflammation; therefore, prevention of secondary infection may be critical in postresuscitation patients. Temporary hyperoxia following hypoxic insult showed no difference in inflammatory reaction compared with hypoxia-normoxia. Rather, temporary hyperoxia may suppress or minimize inflammation by attenuation of TLR receptor.
It is well known that continuous hyperoxygenation after successful cardiac arrest harms patients, but temporary hyperoxygenation with 100% O in a clinical situation may be helpful.
心脏骤停后综合征（PCAS）与脓毒症有许多共同特征，包括血浆细胞因子升高伴细胞因子产生失调以及血浆中存在内毒素。PCAS与缺血-再灌注损伤密切相关。在缺血-再灌注损伤过程中，作为固有免疫第一道防线的中性粒细胞起主要作用。在本研究中，我们在由缺氧-常氧和缺氧-高氧环境模拟的模型中研究了人中性粒细胞的炎症反应。
从全血中分离出中性粒细胞后，将它们分为3个实验组：常氧-常氧组、缺氧-常氧组和缺氧-高氧组。检测中性粒细胞中HO的产生、Toll样受体4（TLR）受体的表达以及中性粒细胞的凋亡程度。
模拟PCAS的缺氧-常氧和缺氧-高氧模型显示，缺氧损伤引发了中性粒细胞的炎症反应。脂多糖会放大这种炎症；因此，预防复苏后患者的继发感染可能至关重要。缺氧损伤后的短暂高氧与缺氧-常氧相比，炎症反应无差异。相反，短暂高氧可能通过减弱TLR受体来抑制或最小化炎症。
众所周知，心脏骤停成功后持续高氧会对患者造成伤害，但在临床情况下使用100%氧气进行短暂高氧可能会有帮助。
