Dexamethasone protects the glycocalyx on the kidney microvascular endothelium during severe acute pancreatitis.

Wen-qiao YU; Shao-yang Zhang; Shui-qiao FU; Qing-hui FU; Wei-na LU; Jian Zhang; Zhong-yan Liang; Yun Zhang; Ting-bo Liang

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Dexamethasone protects the glycocalyx on the kidney microvascular endothelium during severe acute pancreatitis.

Author: Wen-Qiao YU ¹ ; Shao-Yang ZHANG ² ; Shui-Qiao FU ¹ ; Qing-Hui FU ² ; Wei-Na LU ² ; Jian ZHANG ¹ ; Zhong-Yan LIANG ³ ; Yun ZHANG ¹ ; Ting-Bo LIANG ¹
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1. Department of Hepatobiliary and Pancreatic Surgery and Intensive Care Unit, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310021, China.
2. Department of Surgical Intensive Care Unit, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310021, China.
3. Department of Reproductive Medicine, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China.
Publication Type:Journal Article
Keywords: Severe acute pancreatitis (SAP); Acute kidney injury (AKI); Glycocalyx; Dexamethasone; Tumor necrosis factor-α (TNF-α)
MeSH: Acute Disease; Animals; Dexamethasone/pharmacology*; Disease Models, Animal; Edema/metabolism*; Endothelium, Vascular/metabolism*; Enzyme-Linked Immunosorbent Assay; Glycocalyx/drug effects*; Kidney/drug effects*; Male; Mice; Mice, Inbred C57BL; Microcirculation; Pancreatitis/drug therapy*; Perfusion; Protective Agents/pharmacology*; Tumor Necrosis Factor-alpha/metabolism*
From: Journal of Zhejiang University. Science. B 2019;20(4):355-362
CountryChina
Language:English
Abstract: OBJECTIVE:This study demonstrated that dexamethasone (DEX) protects the endothelial glycocalyx from damage induced by the inflammatory stimulus tumor necrosis factor-α (TNF-α) during severe acute pancreatitis (SAP), and improves the renal microcirculation.
METHODS:Ninety mice were evenly divided into 3 groups (Sham, SAP, and SAP+DEX). The SAP mice model was established by ligature of pancreatic duct and intraperitoneal injection of cerulein. Renal perfusion and function, and morphological changes of the glycocalyx were evaluated by laser Doppler velocimetry, electron microscopy, and histopathology (hematoxylin and eosin (H&E) staining), respectively. Serum levels of syndecan-1 and TNF-α were assessed by enzyme-linked immunosorbent assay (ELISA). The protective effects of dexamethasone on the glycocalyx and renal microcirculation were evaluated.
RESULTS:Significantly high levels of serum TNF-α were detected 3 h after the onset of SAP. These levels might induce degradation of the glycocalyx and kidney hypoperfusion, resulting in kidney microcirculation dysfunction. The application of dexamethasone reduced the degradation of the glycocalyx and improved perfusion of kidney.
CONCLUSIONS:Dexamethasone protects the endothelial glycocalyx from inflammatory degradation possibly initiated by TNF-α during SAP. This is might be a significant discovery that helps to prevent tissue edema and hypoperfusion in the future.