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Endothelial glycocalyx injury is involved in heatstroke-associated coagulopathy and protected by N-acetylcysteine.
Peng, Na Geng, Yan Ouyang, Jiafu Liu, Shuai Yuan, Fangfang Chen, Wenda Yu, Baojun Tang, Youqing Su, Lei Liang, Huaping
Peng, Na
Geng, Yan
Ouyang, Jiafu
Liu, Shuai
Yuan, Fangfang
Chen, Wenda
Yu, Baojun
Tang, Youqing
Su, Lei
Liang, Huaping
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Date
06/06/2023
Date Submitted
Keywords
n-Acetylcysteine
coagulopathy
hyaluronic acid
syndecan-1
endothelial glycocalyx
heat stroke
coagulopathy
hyaluronic acid
syndecan-1
endothelial glycocalyx
heat stroke
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fimmu-14-1159195.pdf
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Abstract
Clinical data showed that HS patients complicated with DIC had a higher risk of death than HS patients without DIC. In a rat HS model, we found that rats subjected to heat stress developed hypercoagulability and platelet activation at the core body temperature of 43°C, just before the onset of HS. At 24 h of HS, the rats showed a consumptive hypo-coagulation state. The pulmonary capillary EGCX started to shed at 0 h of HS and became more severe at 24 h of HS. Importantly, pretreatment with NAC substantially alleviated EGCX damage and reversed the hypo-coagulation state in HS rats. Mechanically, HS initiated reactive oxidative species (ROS) generation, while ROS could directly cause EGCX damage. Critically, NAC protected against EGCX injury by attenuating ROS production in heat-stressed or hydrogen peroxide (H2O2)-stimulated endothelial cells.
Language
en
Citation
ISSN
eISSN
1664-3224
ISBN
DOI
10.3389/fimmu.2023.1159195
PMID
37350963
PMCID
PMC10283401