Shedding of the coronary endothelial glycocalyx: effects of hypoxia/reoxygenation vs ischaemia/reperfusion

Annecke, Thorsten; Fischer, Julius; Hartmann, Heike; Tschoep, Johannes; Rehm, Markus; Conzen, Peter; Sommerhoff, Christian P.; Becker, B.F.

doi:10.1093/bja/aer269

Cited by 89 publications

(67 citation statements)

References 35 publications

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“…1 In the present study, we confirmed that ischemia-reperfusion injury can cause degradation of endothelial glycocalyx in liver tissues. 2,8,10,27,28 Pretreatment with sevoflurane significantly reduced the shedding of HS and Syn-1 after the ischemia-reperfusion injury. 12,13 Similarly, the ischemia-reperfusion injury can cause the destruction of the endothelial glycocalyx in the heart tissues of guinea pigs and humans.…”

Section: Discussionmentioning

confidence: 97%

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Yuan

Zhao

et al. 2016

Int J Immunopathol Pharmacol

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The endothelial glycocalyx plays a critical role in the regulation of vascular structure and functions. Previous studies have demonstrated that sevoflurane, a volatile anesthetic, can preserve the endothelial glycocalyx in heart tissues against ischemia-reperfusion injury. However, little is known about the effects of sevoflurane pretreatment on the vascular structure and functions of liver tissues following ischemia-reperfusion injury. To this end, female Sprague-Dawley rats (n = 28) were anesthetized either with ketamine (80-120 mg/kg, i.p.) or with one minimum alveolar concentration (MAC) sevoflurane (2% v/v). Following in vivo hepatic ischemia procedure, the liver was isolated and reperfusion was produced. During the period of reperfusion, liver reperfusion samples were collected, and the concentrations of heparan sulfate and syndecan-1 (Syn-1), and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes, were measured. The morphology of hepatocytes and endothelial glycocalyx were then assessed by using the light and electron microscopies, respectively. Ischemia-reperfusion increased the release of HS and Syn-1, and elevated the levels of ALT and AST in a time-dependent manner. However, sevoflurane pretreatment reduced the release of HS and Syn-1and attenuated the levels of ALT and AST, in a time-dependent manner, as compared with ketamine pretreatment. Furthermore, sevoflurane pretreatment decreased the shedding of endothelial glycocalyx and hepatocytes necrosis. Sevoflurane pretreatment preserved the endothelial glycocalyx in the liver tissue against ischemia-reperfusion injury. The effect appears to help protect hepatocytes against ischemia-reperfusion-induced necrosis.

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Section: Discussionmentioning

confidence: 97%

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Yuan

Zhao

et al. 2016

Int J Immunopathol Pharmacol

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“…These studies disclose only one part of the problemddegradation of heparan sulfate moieties, which, however, were shown to be dispensable for the maintenance of the barrier properties of glycocalyx. 18 Annecke et al 19 proposed that the loss of glycocalyx is initiated by the purine metabolite-induced degranulation of resident mast cells and release of tryptase b acting as a sheddase. The instantaneous dilution of tryptase b in the bloodstream should, however, reduce the impact of this factor on ESG.…”

Section: Discussionmentioning

confidence: 99%

Exocytosis of Endothelial Lysosome-Related Organelles Hair-Triggers a Patchy Loss of Glycocalyx at the Onset of Sepsis

Zullo

Fan

Azar

et al. 2016

The American Journal of Pathology

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Sepsis is a systemic inflammatory syndrome induced by bacterial infection that can lead to multiorgan failure. Endothelial surface glycocalyx (ESG) decorating the inner wall of blood vessels is a regulator of multiple vascular functions. Here, we tested a hypothesis that patchy degradation of ESG occurs early in sepsis and is a result of exocytosis of lysosome-related organelles. Time-lapse video microscopy revealed that exocytosis of Weibel-Palade bodies and secretory lysosomes occurred a few minutes after application of lipopolysaccharides to endothelial cells. Two therapeutic maneuvers, a nitric oxide intermediate, NG-hydroxy-L-arginine, and culture media conditioned by endothelial progenitor cells reduced the motility of lysosome-related organelles. Confocal and stochastic optical reconstruction microscopy confirmed the patchy loss of ESG simultaneously with the exocytosis of lysosome-related organelles and Weibel-Palade bodies in cultured endothelial cells and mouse aorta. The loss of ESG was blunted by pretreatment with NG-hydroxy-L-arginine or culture media conditioned by endothelial progenitor cells. Moreover, these treatments resulted in a significant reduction in deaths of septic mice. Our data support the hypothesis assigning to stress-induced exocytosis of these organelles the role of a hair-trigger for local degradation of ESG that initiates leukocyte infiltration, increase in vascular permeability, and partially accounts for the later rates of morbidity and mortality. Sepsis is a systemic inflammatory syndrome induced by bacterial infection that can lead to multiorgan failure. It afflicts >700,000 individuals annually in the United States alone, has mortality rates of 30%, and is the 11th leading cause of death. One of the key molecular causes of Gram-negative septicemia is endotoxin that consists of lipopolysaccharides (LPSs) bound with high affinity to LPS-binding glycoprotein. Complex LPS-binding glycoprotein is recognized by cognate receptor Toll-like receptor 4 and co-receptor CD14 on monocytes/macrophages and endothelial cells. 1 Considering the systemic nature of septicemia, vascular endothelium represents the first line of exposure to bacterial endotoxins. 2 It responds to endotoxins with a complex system of danger signals, which are chronologically sequenced and spatially propagated. 3 Functionally, these waves of danger signaling tend to secure proper organismal responses, both proinflammatory and anti-inflammatory.Among the earliest responses of activated endothelial cells to endotoxin are exocytosis of Weibel-Palade bodies (WPBs) and secretory lysosomes. 4 WPBs are rod-shaped members of lysosome-related organelles (0.2 mm by 2 to 3

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“…Endothelial cytoskeletal derangement and hypercontracture induce gap formation, [68][69][70][71] which is enhanced by extracellular adenosine but attenuated by extracellular ATP. 72 Degradation of the glycocalyx also contributes to reduced endothelial barrier function and edema formation 66,73,74 ; tumor necrosis factor α is an important mediator of glycocalyx degradation, 75 and glycocalyx degradation also promotes leukocyte 76 and platelet adherence. 77 Exogenous nitric oxide preserves vascular integrity and attenuates edema formation through protection of the glycocalyx.…”

Section: Vascular Permeability: Edemamentioning

confidence: 99%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

209

160

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Abstract:The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/ reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre-and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available. (Circ Res.

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Shedding of the coronary endothelial glycocalyx: effects of hypoxia/reoxygenation vs ischaemia/reperfusion

Abstract: Both ischaemic and hypoxic hypoxia initiate glycocalyx degradation, promoting an increase in permeability. A contributing mechanism could be purine-mediated degranulation of resident mast cells, with liberated tryptase β acting as potential 'sheddase'.

Cited by 89 publications

References 35 publications

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Exocytosis of Endothelial Lysosome-Related Organelles Hair-Triggers a Patchy Loss of Glycocalyx at the Onset of Sepsis

The Coronary Circulation as a Target of Cardioprotection

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