The inflammatory response of neutrophils in an in vitro model that approximates the postcardiac arrest state

Young-Duck Cho; Sung-Jun Park; Sung-Hyuk Choi; Young-Hoon Yoon; Jung-Youn Kim; Sung-Woo Lee; Chae-Seung Lim

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저자정보: Young-Duck Cho (Korea University College of Medicine) Sung-Jun Park (Korea University) Sung-Hyuk Choi (Korea University) Young-Hoon Yoon (Korea University College of Medicine) Jung-Youn Kim (Korea University College of Medicine) Sung-Woo Lee (Korea University College of Medicine) Chae-Seung Lim (Korea University College of Medicine)

저널정보: 대한외과학회 Annals of Surgical Treatment and Research Annals of Surgical Treatment and Research Vol.93 No.4

발행연도: 2017.10

수록면: 217 - 224 (8page)

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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: normoxianormoxia, 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.

#Neutrophil #Reperfusion injury #Hypoxia #Hyperoxia

참고문헌 (27)

참고문헌 신청

[학술지(정기간행물)] - Negovsky VA. / 1972 / The second step in resuscitation--the treatment of the ‘post-resuscitation disease’ / Resuscitation 1 : 1 ~ 7

[학술지(정기간행물)] - Adrie C / 2002 / Successful cardiopulmonary resuscitation after cardiac arrest as a"sepsis-like"syndrome / Circulation 106 : 562 ~ 568

[학술지(정기간행물)] - Ar’Rajab A / 1996 / Reperfusion injury / New Horiz 4 : 224 ~ 234

[학술지(정기간행물)] - Strieter RM / 1992 / Cytokine-induced neutrophil-derived interleukin-8 / Am J Pathol 141 : 397 ~ 407

[학술지(정기간행물)] - Adrie C / 2004 / Spaulding C. Postresuscitation disease after cardiac arrest: a sepsis-like syndrome? / Curr Opin Crit Care 10 : 208 ~ 212

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