Hemorrhagic Shock and Resuscitation Causes Glycocalyx Shedding and Endothelial Oxidative Stress Preferentially in the Lung and Intestinal Vasculature.

Autor:	Abdullah S; Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana., Karim M; Tulane University School of Medicine, New Orleans, Louisiana., Legendre M; Department of Chemical and Biomolecular Engineering, University of Notre Dame, Notre Dame, Indiana., Rodriguez L; Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana., Friedman J; Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana., Cotton-Betteridge A; Tulane University School of Medicine, New Orleans, Louisiana., Drury R; Tulane University School of Medicine, New Orleans, Louisiana., Packer J; Tulane University School of Medicine, New Orleans, Louisiana., Guidry C; Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana., Duchesne J; Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana., Taghavi S; Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana., Jackson-Weaver O; Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana.
Jazyk:	angličtina
Zdroj:	Shock (Augusta, Ga.) [Shock] 2021 Nov 01; Vol. 56 (5), pp. 803-812.
DOI:	10.1097/SHK.0000000000001764
Abstrakt:	Introduction: Hemorrhagic shock has recently been shown to cause shedding of a carbohydrate surface layer of endothelial cells known as the glycocalyx. This shedding of the glycocalyx is thought to be a mediator of the coagulopathy seen in trauma patients. Clinical studies have demonstrated increases in shed glycocalyx in the blood after trauma, and animal studies have measured glycocalyx disruption in blood vessels in the lung, skeletal muscle, and mesentery. However, no study has measured glycocalyx disruption across a wide range of vascular beds to quantify the primary locations of this shedding. Methods: In the present study, we used a rat model of hemorrhagic shock and resuscitation to more comprehensively assess glycocalyx disruption across a range of organs. Glycocalyx disruption was assessed by fluorescent-labeled wheat germ agglutinin or syndecan-1 antibody staining in flash frozen tissue. Results: We found that our model did elicit glycocalyx shedding, as assessed by an increase in plasma syndecan-1 levels. In tissue sections, we found that the greatest glycocalyx disruption occurred in vessels in the lung and intestine. Shedding to a lesser extent was observed in vessels of the brain, heart, and skeletal muscle. Liver vessel glycocalyx was unaffected, and kidney vessels, including the glomerular capillaries, displayed an increase in glycocalyx. We also measured reactive oxygen species (ROS) in the endothelial cells from these organs, and found that the greatest increase in ROS occurred in the two beds with the greatest glycocalyx shedding, the lungs, and intestine. We also detected fibrin deposition in lung vessels following hemorrhage-resuscitation. Conclusions: We conclude that the endothelium in the lungs and intestine are particularly susceptible to the oxidative stress of hemorrhage-resuscitation, as well as the resulting glycocalyx disruption. Thus, these two vessel beds may be important drivers of coagulopathy in trauma patients. Competing Interests: The authors report no conflicts of interest. (Copyright © 2021 by the Shock Society.)
Databáze:	MEDLINE
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