AUGMENTATION OF PLATELET AND ENDOTHELIAL CELL eNOS ACTIVITY DECREASES SEPSIS-RELATED NEUTROPHIL-ENDOTHELIAL CELL INTERACTIONS

@article{Khan2010AUGMENTATIONOP,
  title={AUGMENTATION OF PLATELET AND ENDOTHELIAL CELL eNOS ACTIVITY DECREASES SEPSIS-RELATED NEUTROPHIL-ENDOTHELIAL CELL INTERACTIONS},
  author={Raymond Khan and Linda A. Kirschenbaum and Catherine Larow and Gioiamaria B. Berna and Kelly Griffin and Mark E. Astiz},
  journal={Shock},
  year={2010},
  volume={33},
  pages={242-246}
}
NO is an important mediator of microvascular patency and blood flow. The purpose of this study was to examine the role of enhanced eNOS activity in attenuating sepsis-induced neutrophil-endothelial cell interactions. Microslides coated with human umbilical vein endothelial cells were stimulated with plasma from patients with septic shock. Neutrophil and platelets from control subjects were also stimulated with plasma from patients in septic shock and perfused over stimulated endothelial cells… 

Effect of Ascorbate on Coagulation and Fibrinolytic Factors in the Septic Microvasculature

It is observed that sepsis-induced increases in bacterial count, PAI-1 expression and myeloperoxidase content in various organs were not affected by ascorbate, suggesting that the lack of effect of asCorbate on PAi-1 in the tissue may maintain PAI’1’s beneficial role insepsis.

Vascular endothelial dysfunction and pharmacological treatment.

  • J. Su
  • Biology, Medicine
    World journal of cardiology
  • 2015
Experimental and clinical studies have demonstrated that a variety of currently used or investigational drugs, such as angiotensin-converting enzyme inhibitors, ang Elliotensin AT1 receptors blockers, angiotENSin-(1-7), antioxidants, beta-blockers, calcium channel blockers, endothelial NO synthase enhancers, phosphodiesterase 5 inhibitors, sphingosine-1-phosphate and statins, exert endothelial protective effects.

Vascular endothelial dysfunction and pharmacological treatment

Experimental and clinical studies have demonstrated that a variety of currently used or investigational drugs, such as angiotensin-converting enzyme inhibitors, ang Elliotensin AT1 receptors blockers, angiotENSin-(1-7), antioxidants, beta-blockers, calcium channel blockers, endothelial NO synthase enhancers, phosphodiesterase 5 inhibitors, sphingosine-1-phosphate and statins, exert endothelial protective effects.

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The β-common receptor (βcR) plays a pivotal role in the nonhematopoietic tissue-protective effects of erythropoietin (EPO). Here we determined whether EPO reduces the acute kidney injury (AKI) caused

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Ascorbate Reduces Mouse Platelet Aggregation and Surface P‐Selectin Expression in an Ex Vivo Model of Sepsis

It is hypothesized that ascorbate reduces aggregation of platelets and their surface expression of P‐selectin (a key adhesion molecule) in mice in a manner that prevents plugging in septic capillaries.

Sepsis-induced cardiac dysfunction: Pathophysiology and experimental treatments

It is demonstrated for the first time that the cardiac dysfunction caused by sepsis was less pronounced in female than in male mice; this protection was associated with cardiac activation of a pro-survival pathway [Akt and endothelial nitric oxide synthase], and the decreased activation of an pro-inflammatory signalling pathway [nuclear factor (NF)-κB].

Novel biomarkers for early prediction of sepsis-induced disseminated intravascular coagulation in a mouse cecal ligation and puncture model

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Endothelial nitric oxide synthase 894G→T but not -786T→C gene polymorphism is associated with organ dysfunction and increased mortality in patients with severe sepsis.

It is found that the eNOS -786T→C polymorphism was not associated with severity of disease or mortality of patients with sepsis, and the GT genotype (894G→T) was associated with the occurrence of shock and impaired organ function.

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