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The impacts of oxygen and pentoxifylline in hypoxic condition.

Authors :
Young-Duck Cho
Sung-Hyuk Choi
Sung-Jun Park
Jung-Youn Kim
Chae-Seung Lim
Woo-Sung Yu
Kim Kyung Hwan
Tae-Gun Shin
Source :
European Journal of Inflammation. 1/1/2022, Vol. 20, p1-10. 10p.
Publication Year :
2022

Abstract

Introduction:Among major trauma patients in the emergency department, the leading cause of morbidity and mortality is a hemorrhagic shock. The low oxygen flow with hypovolemia in trauma patients is believed to play a significant role. Hence, oxygen supply is essential in severe trauma patients with massive hemorrhage. This study aimed to investigate the effect of oxygen supply in hypoxic condition and variable treatments such as pentoxifylline (PTX), glycerol, hypertonic saline (HTS), protease inhibitor, and dexamethasone (DEXA) in macrophage and T cells. Method:Nitric oxide synthase (iNOS) and macrophage migration inhibitory factor (MIF) were measured for macrophage. MIF, interleukin (IL)-2, and IL-8 were measured for T cells. T cell viability was measued by MTT assay. Results: Pentoxifylline decreased iNOS expression mostly followed by glycerol under hypoxia. Under the hyperoxia, PTX and other treatments decreased iNOS expressions in macrophage. MIF expression was lowered with PTX under hypoxia. PTX, glycerol, HTS, and protease inhibitor were effective under hyperoxia in macrophage. PTX increased T cell survival under hypoxia. Under the hyperoxia, IL-2 expressions were upregulated with PTX, glycerol, and HTS. PTX and other treatments were effective for IL-8. Our results indicate that the PTX and the other agents tested reversed the effects of stimulation of lipopolysaccharide, PGE2 in hypoxia or hypoxia. Conclusion:Our study demonstrated potential usefulness in improving immune systems during severe inflammatory conditions similar to septic shock possibly caused by massive hemorrhage. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
1721727X
Volume :
20
Database :
Academic Search Index
Journal :
European Journal of Inflammation
Publication Type :
Academic Journal
Accession number :
161998359
Full Text :
https://doi.org/10.1177/20587392211056508