The inflammatory response of neutrophils in an in vitro model that approximates the postcardiac arrest state.
10.4174/astr.2017.93.4.217
- Author:
Young Duck CHO
1
;
Sung Jun PARK
;
Sung Hyuk CHOI
;
Young Hoon YOON
;
Jung Youn KIM
;
Sung Woo LEE
;
Chae Seung LIM
Author Information
1. Department of Emergency Medicine, Korea University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Neutrophil;
Reperfusion injury;
Hypoxia;
Hyperoxia
- MeSH:
Anoxia;
Apoptosis;
Coinfection;
Heart Arrest;
Humans;
Hyperoxia;
Immunity, Innate;
In Vitro Techniques*;
Inflammation;
Neutrophils*;
Passive Cutaneous Anaphylaxis;
Plasma;
Reperfusion Injury;
Sepsis;
Toll-Like Receptor 4
- From:Annals of Surgical Treatment and Research
2017;93(4):217-224
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: 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 in vitro model which we simulated with hypoxia-normoxia and hypoxia-hyperoxia environments. METHODS: 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 H₂O₂, the expression of Toll-like receptor 4 (TLR₄) receptor, and the extent of apoptosis of the neutrophils were checked. RESULTS: The in vitro 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 TLR4 receptor. CONCLUSION: It is well known that continuous hyperoxygenation after successful cardiac arrest harms patients, but temporary hyperoxygenation with 100% O₂ in a clinical situation may be helpful.
