Corpus ID: 79288596

Glicocálix. Una estructura a considerar en el enfermo grave

  title={Glicoc{\'a}lix. Una estructura a considerar en el enfermo grave},
  author={R. C. Esper and A. Mendoza and Oscar Iv{\'a}n Flores Rivera and Alejandro D{\'i}az-Gir{\'o}n Gidi and Itzel Monserrat at Gonz{\'a}lez Mart{\'i}nez and Diego Araiza Garaygordobil},
RESUMEN Las células endoteliales conforman el recubrimiento interno del corazón, vasos sanguíneos y linfáticos. La porción apical de las células endoteliales contiene glicocálix, una red compleja de macromoléculas, incluyendo proteínas de unión, proteoglicanos y glicoproteínas. Esta compleja red recubre las células endoteliales y sus hendiduras en su segmento luminal. El glicocálix tiene un papel fundamental en la fi siología microvascular y endotelial, en particular, en la regulación del tono… Expand
1 Citations
Eficacia de los niveles de albúmina como marcador de mortalidad en pacientes sépticos en el Hospital Teodoro Maldonado Carbo del 1 de enero al 31 de diciembre de 2017.
Por cada gramo de albumina serica that disminuye aumenta the mortalidad del paciente septico, y en aquellos que tengan como antecedentes diabetes mellitus tipo 2 e insuficiencia renal cronica ya que son los mas propensos al desarrollo of esta patologia. Expand


Inflammation- and ischemia-induced shedding of venular glycocalyx.
The composition of the glycocalyx results from a balance of the rate of biosynthesis of GAGs by the endothelial cell and their shedding, which may be mediated by intracellular and/or membrane-bound proteases or lyases released or activated by G protein signaling. Expand
Sepsis and major abdominal surgery lead to flaking of the endothelial glycocalix.
High levels of glycocalIX markers indicated that significant flaking of the endothelial glycocalix occurred in patients with sepsis, and to a lesser extent in patients after major abdominal surgery, which could explain the nonspecific capillary leaking syndrome of patients withSepsis and after major abdomen surgery. Expand
Regulation of Microvascular Thromboembolism In Vivo
This review focus is on the endothelial regulation of platelet‐vessel wall interactions during thromboembolism in vivo, paying special attention to the endothelium‐derived platelet inhibiting substances nitiric oxide and prostacyclin and to differences between arteriolar and venular endot Helium. Expand
Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo.
A potential role for glycocalyx perturbation in mediating vascular dysfunction during hyperglycemia is indicated, thereby increasing vascular vulnerability and indicating a potential roles for N-acetylcysteine and mannitol infusion. Expand
Endothelial Glycocalyx as an Additional Barrier Determining Extravasation of 6% Hydroxyethyl Starch or 5% Albumin Solutions in the Coronary Vascular Bed
The endothelial glycocalyx acts as a competent barrier for water and colloids and only after its destruction do changes in endothelial morphology (postischemic reperfusion or histamine application) become effective determinants of coronary extravasation. Expand
The endothelial glycocalyx: a potential barrier between health and vascular disease
Cumulating evidence suggests that an intact glycocalyx protects the vessel wall, whereas disruption of the glycocalyX upon atherogenic stimuli increases vascular vulnerability for atherogenesis. Expand
Especially polymorphonuclear leukocytes, but also monomorphonuclear leukocytes, roll spontaneously in venules of intact rat skin: involvement of E-selectin.
Most of the leukocytes rolling spontaneously in postcapillary venules of intact rat skin are granulocytes, despite the absence of an acute inflammatory reaction, one of the adhesion molecules involved in this phenomenon is E-selectin. Expand
Reactive oxygen species mediate modification of glycocalyx during ischemia-reperfusion injury.
The liability of GcX during I/R injury is demonstrated; the importance of locally produced ROS in the injury to Gcx is shown; and the potential importance of heparin-binding sites in modulating the ROS production is highlighted. Expand
Ischemia/reperfusion-induced microvascular dysfunction: role of oxidants and lipid mediators.
The hypothesis that oxidants produced, in part, by xanthine oxidase promote the formation (by mast cells and endothelial cells) of platelet-activating factor and leukotriene B4, which recruit and activate leukocytes in postcapillary venules is supported. Expand
Role of hyaluronic acid glycosaminoglycans in shear-induced endothelium-derived nitric oxide release.
It is concluded that hyaluronic acid glycosaminoglycans within the glycocalyx play a pivotal role in detecting and amplifying the shear force of flowing blood that triggers endothelium-derived NO production in isolated canine femoral arteries. Expand