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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 #68653
Title: IN VIVO PLATELET THROMBUS FORMATION IN MICROVESSELS OF COPPER DEFICIENT RATS

Author
item LOMINADZE, D - U LOUISVILLE
item Saari, Jack
item MILLER, F - U LOUISVILLE
item SCHUSCHKE, D - U LOUISVILLE

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 8/25/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: We have previously shown that dietary copper restriction reduces thrombogenesis and hemostasis in rat microcirculation. In the present study, the role of shear forces in in vivo thrombus formation was examined in the cremaster muscle microcirculation of copper deficient rats. Male, weanling Sprague-Dawley rats were fed purified diets for 4 weeks that were either copper-adequate (CuA, 6.3 ug Cu/g diet) or copper deficient (CuD, 0.3 ug Cu/g diet). Fluorescein isothiocyanate tagged to bovine serum albumin (FITC-BSA) was injected i.a. and 450-490 nm light was used to activate the FITC-BSA and induce a thrombus that was observed with in vivo television microscopy. Measurements were made in third order arterioles and venules in which mean wall shear rates were 523+/-53 s**-1 and 321+/- 23 s**-1 respectively. The time to the start of thrombogenesis in CuD rats in both arterioles and venules was significantly prolonged. However, once the thrombus had started, it took less time for complete occlusion of the vessels in the CuD rats. Greater shear rates in arterioles versus venules increased the thrombus initiation time in both CuA and CuD groups. However, vessel occlusion time and time for platelet thrombus growth following initiation between these groups were independent of shear rate. The absence of an interaction between copper status and vessel type on measured variables suggests that decreased thrombogenesis in copper deficiency is not a result of altered rheological factors or a property of the vessel wall (that can be represented by arteriolar-venular differences). It apparently results from decreased platelet-to- endothelial cell adhesion. Supported by USDA agreement 95-37200-1625.