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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #76840
Title: VON WILLEBRAND FACTOR RESTORES IMPAIRED PLATELET THROMBOGENESIS IN COPPER- DEFICIENT RATS

Author
item LOMINADZE, DAVID - U LOUISVILLE
item Saari, Jack
item MILLER, FREDERICK - U LOUISVILLE
item CATALFAMO, JAMES - CORNELL UNIVERSITY
item SCHUSCHKE, DALE - U LOUISVILLE

Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/25/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary: Prevention of blood loss from an injured blood vessel requires that platelets (cells circulating in the blood) adhere to the vessel wall at the site of injury and then adhere to one another to form a clot. This process depends on a cascade of reactions between chemical and physical factors that reside in the blood, inside the platelets and in cells of the vessel wall. Clotting is known to be impaired in dietary copper deficiency. Previous studies have shown that aggregation of platelets to one another is increased and adhesion of platelets to cells of the blood vessel wall is decreased in copper deficiency and that these events are accompanied by alteration of chemical clotting factors. The purpose of this study was to examine the effect of physical factors on clotting in copper deficiency. This was done by observing the change in speed of clotting when flow rate in a vessel was reduced by partially blocking the vessel. We found that the speed of clotting was reduced when flow rate was reduced but that the percentage reduction was not influenced by copper deficiency. This suggests that altered physical factors do not contribute to the alteration of clotting caused by dietary copper deficiency. This information will be useful to scientists and consumers interested in trace element nutrition of the cardiovascular system.

Technical Abstract: Dietary copper restriction reduces microvascular thrombogenesis. We now examined the roles of shear forces and von Willebrand factor (vWF) on in vivo thrombus formation in the cremaster muscle microcirculation of copper-deficient rats. Male, weanling Sprague-Dawley rats were fed purified diets that were either copper-adequate (6.3 ug Cu/g) or copper- deficient (0.3 ug Cu/g) for 4 weeks. Fluorescein isothiocyanate tagged to bovine serum albumin was injected i.a. and activated with 450-490 nm light to induce thrombus formation. Measurements were made in third order microvessels with mean wall shear rates of 1972 +/- 39 s**-1 or 523 +/- 53 s**-1 in arterioles and 302 +/- 6 s**-1 or 154 +/- 8 s**-1 in venules. In other experiments, thrombogenesis was compared before and after intravascular injection of vWF. The thrombus initiation time was significantly prolonged in copper-deficient rats, but after thrombus appearance, vessel occlusion was more accelerated. Greater shear rates increased the thrombus initiation time in both dietary groups. However, vessel occlusion time and thrombus growth time in groups were independent of shear rate. vWF decreased thrombus initiation time without affecting platelet aggregation. The absence of an interaction between copper status and vessel type or shear forces suggests that decreased thrombogenesis in copper deficiency is not a result of altered rheological factors or arteriolar-venular differences. It apparently is the result of decreased platelet-to-endothelial cell adhesion.