1999
DOI: 10.1016/s0049-3848(99)00013-4
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Plasma von Willebrand Factor and Intestinal Ischaemia-Reperfusion Injury in Rats

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Cited by 6 publications
(7 citation statements)
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“…In agreement with our data, other authors demonstrated in rats that the plasma concentration of vWF rose after 30 min of intestinal ischemia followed by 15 min of reperfusion (2). Moreover, hypoxia, and also reoxygenation, induced release of vWF endothelial secretory granules in cultured cells (30).…”
Section: Discussionsupporting
confidence: 93%
See 1 more Smart Citation
“…In agreement with our data, other authors demonstrated in rats that the plasma concentration of vWF rose after 30 min of intestinal ischemia followed by 15 min of reperfusion (2). Moreover, hypoxia, and also reoxygenation, induced release of vWF endothelial secretory granules in cultured cells (30).…”
Section: Discussionsupporting
confidence: 93%
“…After treatment, the diameter, RBC velocity, and flow changes in arterioles were evaluated, as well as plasma lipid peroxidation, vascular permeability, leukocyte adhesion, and changes in perfused capillary length (PCL) (4,7). Experiments were also carried out to measure the influence of I/R, with and without treatment, on plasma vWF concentration (2). To investigate the mechanisms contributing to the effects of the PEG compounds, the hamster cheek pouch was treated with the NO synthase inhibitor N Gmonomethyl-L-arginine (L-NMMA) in addition to PEG-NO before I/R.…”
mentioning
confidence: 99%
“…The vWF factor contributes to primary hemostasis by facilitating platelet attachment to subendothelial substances in an injured vessel wall, stimulating the formation of a primary platelet plug. In the circulation, vWF protects factor VIII from proteolysis, and also serves to direct F VIII to sites in need of hemostasis (1,2,15,16). With its multi-adhesive properties vWF is able to bind a number of different proteins (1).…”
Section: Discussionmentioning
confidence: 99%
“…Many mechanisms and factors trigger the acute release of vWF from endothelial cells: α-thrombin, plasminogen activator, plasmin, adrenalin, bradykinin, interleukin-1 and calcium ionophore all increase its release (1,15,16). Usually the mechanism of increase in the vWF level involves an increase of acute phase proteins, or is a result of endothelial injury (1,6,15,16). In our study vWF release was unrelated to the endothelial cell trauma induced by cryopexy, but there was a tendency to lower values of this factor in SRF before cryopexy.…”
Section: Discussionmentioning
confidence: 99%
“…Increased levels of vWF have been associated with CAD (4) and acute coronary syndromes (5,6). Chronic smoking may be associated with increased levels of vWF (28), possibly due to its release during oxidative damage of endothelial cells (29). Therefore, combined, high-dose antioxidant treatment may reduce vWF levels four weeks.…”
Section: Vwfmentioning
confidence: 99%