Oxidized Lipoproteins Degrade the Endothelial Surface Layer

Vink, Hans; Constantinescu, Alina A.; Spaan, Jos A. E.

doi:10.1161/01.cir.101.13.1500

Cited by 344 publications

(167 citation statements)

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“…Surgical stress or stress from tissue hypoxia as a result of a reduction in DO 2 due to a hemorrhagic shock leads to the liberation of inflammatory mediators [14][15][16] , which provokes a reduction in endothelial glycocalyx and leads to an increase in platelet aggregation 17 , leukocyte adhesion to the endothelial surface 18 and endothelial permeability, causing tissue edema [19][20] .…”

Section: Discussionmentioning

confidence: 99%

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Effects of catecholamines on volemic replacement with saline solution and the impact on heart rate variability in rabbits subjected to hemorrhage. A study by spectral analysis

et al. 2014

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PURPOSE: To verify the effects of different catecholamines on volemic expansion and on the autonomic nervous system in rabbits that were subjected to hemorrhage. METHODS:Twenty four rabbits subjected to hemorrhage (with a 25% loss of blood volume) and were randomly divided into four experimental groups: 1) HEMO Group underwent replacement with their own blood in an equal volume; 2) SS Group underwent replacement with saline solution (SS) in a volume that corresponded to three times the removed blood volume; 3) ISP Group underwent replacement with SS and isoprenaline; 4) FNL Group underwent replacement with SS and phenylephrine. Spectral Analysis of the heart rate and heart rate variability were performed from the recorded data. Hematocrit was measured throughout the experiment. RESULTS:Replacement with SS and an α-or β-agonist did not produce differences in the intravascular retention compared to replacement with SS alone. An analysis of HRV showed that the FNL group maintained the LF/HF ratio better than ISP and SS. CONCLUSIONS:No difference in vascular retention when α-or β-agonists were added to SS during post-hemorrhagic recovery. The animals in the FNL group maintained the integrity of the autonomic response within normal physiological standards during hemorrhagic stress.

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Section: Discussionmentioning

confidence: 99%

“…According to experimental ischemia-reperfusion studies [19][20][21] , proteases 11 , tumor necrosis factor alpha 22 , free oxygen radicals 17 and atrial natriuretic peptide degrade the endothelial glycocalyx.…”

Section: Discussionmentioning

confidence: 99%

Effects of catecholamines on volemic replacement with saline solution and the impact on heart rate variability in rabbits subjected to hemorrhage. A study by spectral analysis

et al. 2014

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“…A common mechanism of damaging effect renders oxidative stress a dominating factor in the development of various cardiovascular disorders [39,40]. Excessive ROS generation leads to destruction of endothelial glycocalyx [41]. To prevent and reduce this damage the glycocalyx accumulates antioxidants e.g., extracellular superoxide dismutase (exSOD, Figure 4).…”

Section: Glycocalyx and Reactive Oxygen Speciesmentioning

confidence: 99%

Translational research into vascular wall function: regulatory effects of systemic and specific factors

Maksimenko¹

2017

J Transl Sci

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Development of biomedical techniques has intensified the investigation of endothelial glycocalyx as an individual research object. The effect of vascular wall hydration on progression of pathological lesions, including atherosclerosis, has been revealed and examined. There is evidence that atherosclerosis is associated with water-sulfate and water-sodium exchange. The concept that atherosclerosis is initiated by deficiency of sulfur-containing compounds has been regarded. Glycocalyx protective function against damaging effect of oxidative stress on vascular wall is associated with accumulation and retention of antioxidants on luminal surface of blood vessel. The review deals with protective activity of antioxidant enzyme derivatives, computational methods to determine the principles of the glycocalyx functioning and modeling of the glycocalyx interaction with systemic and specific factors. A limiting influence of crosswind move from clinical practice to life science and contrariwise from life science to clinical practice on the development of translational medicine is emphasized.Abbreviations:

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“…The release of inflammatory mediators induces morphological changes of the endothelium and its protective glycocalyx 30, 31. Endothelial exposure to oxidative stress, oxidized lipoproteins,32, 33, 34 and hyperglycemia35 cause further glycocalyx injury which in turn give rise to profound changes in capillary flows and hematocrit 33, 36. The glycocalyx constitutes a fluid barrier, and degradation of the glycocalyx is hence associated with edema and capillary compression 37, 38…”

Section: The Origins Of Capillary Flow Disturbances or Occlusion In Smentioning

confidence: 99%

Microcirculatory dysfunction and tissue oxygenation in critical illness

Østergaard

Granfeldt

Secher

et al. 2015

Acta Anaesthesiol Scand

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Severe sepsis is defined by organ failure, often of the kidneys, heart, and brain. It has been proposed that inadequate delivery of oxygen, or insufficient extraction of oxygen in tissue, may explain organ failure. Despite adequate maintenance of systemic oxygen delivery in septic patients, their morbidity and mortality remain high.The assumption that tissue oxygenation can be preserved by maintaining its blood supply follows from physiological models that only apply to tissue with uniformly perfused capillaries. In sepsis, the microcirculation is profoundly disturbed, and the blood supply of individual organs may therefore no longer reflect their access to oxygen.We review how capillary flow patterns affect oxygen extraction efficacy in tissue, and how the regulation of tissue blood flow must be adjusted to meet the metabolic needs of the tissue as capillary flows become disturbed as observed in critical illness. Using the brain, heart, and kidney as examples, we discuss whether disturbed capillary flow patterns might explain the apparent mismatch between organ blood flow and organ function in sepsis. Finally, we discuss diagnostic means of detecting capillary flow disturbance in animal models and in critically ill patients, and address therapeutic strategies that might improve tissue oxygenation by modifying capillary flow patterns.

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Oxidized Lipoproteins Degrade the Endothelial Surface Layer

Abstract: Oxygen-derived free radicals mediate the disruption of the EC surface layer and increase vascular wall adhesiveness by Ox-LDL.

Cited by 344 publications

References 9 publications

Effects of catecholamines on volemic replacement with saline solution and the impact on heart rate variability in rabbits subjected to hemorrhage. A study by spectral analysis

Effects of catecholamines on volemic replacement with saline solution and the impact on heart rate variability in rabbits subjected to hemorrhage. A study by spectral analysis

Translational research into vascular wall function: regulatory effects of systemic and specific factors

Microcirculatory dysfunction and tissue oxygenation in critical illness

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