Von Willebrand factor restores impaired platelet thrombogenesis in copper-deficient rats

Dietary copper restriction reduces microvascular thrombogenesis. We have now examined the roles of shear forces and von Willebrand factor (vWF) in in vivo thrombus formation in the cremaster microcirculation of copper-deficient rats. Male weanling Sprague-Dawley rats were fed purified diets that wer...

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Veröffentlicht in:The Journal of nutrition 1997-07, Vol.127 (7), p.1320-1327
Hauptverfasser: Lominadze, David, Saari, Jack T, Miller, Frederick N, Catalfamo, James L, Schuschke, Dale A
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container_issue 7
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container_title The Journal of nutrition
container_volume 127
creator Lominadze, David
Saari, Jack T
Miller, Frederick N
Catalfamo, James L
Schuschke, Dale A
description Dietary copper restriction reduces microvascular thrombogenesis. We have now examined the roles of shear forces and von Willebrand factor (vWF) in in vivo thrombus formation in the cremaster microcirculation of copper-deficient rats. Male weanling Sprague-Dawley rats were fed purified diets that were either copper-adequate (6.3 mg Cu/kg) or copper-deficient (0.3 mg Cu/kg) for 4 wk. Intravascular fluorescein isothiocyanate tagged to bovine serum albumin was activated with 450-490 nm light to induce thrombus formation in microvessels. Thrombus initiation time was significantly prolonged in copper-deficient rats; after thrombus appearance, however, vessel occlusion was significantly accelerated. The greater shear rates of arterioles compared with venules significantly increased the thrombus initiation time in both groups. However, vessel occlusion time and thrombus growth time were independent of shear rate. Intravascular vWF (0.2 u/100 g body wt) decreased thrombus initiation time in the CuD group without affecting thrombus growth time. The data suggest that decreased thrombogenesis in copper-deficient rats is not a result of altered rheological factors or arteriolar-venular differences, but appears to result from decreased platelet-to-endothelial cell adhesion.
doi_str_mv 10.1093/jn/127.7.1320
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The data suggest that decreased thrombogenesis in copper-deficient rats is not a result of altered rheological factors or arteriolar-venular differences, but appears to result from decreased platelet-to-endothelial cell adhesion.</abstract><cop>Bethesda, MD</cop><pub>American Society for Nutritional Sciences</pub><pmid>9202086</pmid><doi>10.1093/jn/127.7.1320</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Analysis of Variance
animal models
Animals
arteries
Arterioles - cytology
Arterioles - physiology
Biological and medical sciences
Blood
blood coagulation factors
blood plasma
blood platelets
Blood Platelets - cytology
Blood Platelets - drug effects
Blood Platelets - physiology
blood pressure
Blood Pressure - physiology
Blood Viscosity - physiology
body weight
Body Weight - physiology
Cell Adhesion - drug effects
Cell Adhesion - physiology
Circulatory system
Copper
Copper - analysis
Copper - deficiency
Copper - physiology
diet
duration
Endothelium, Vascular - cytology
Endothelium, Vascular - physiology
experimental diets
heart rate
Heart Rate - physiology
Hematocrit
Iron - analysis
liver
Liver - chemistry
Male
Medical sciences
Metabolic diseases
nutrient deficiencies
Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)
Rats
Rats, Sprague-Dawley
Regional Blood Flow
Rodents
shear
thrombosis
Thrombosis - blood
Thrombosis - etiology
Thrombosis - physiopathology
trace element deficiencies
veins
viscosity
von Willebrand Factor - pharmacology
title Von Willebrand factor restores impaired platelet thrombogenesis in copper-deficient rats
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