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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 #66084
Title: EFFECT OF SHEAR FORCES ON PLATELET THROMBUS FORMATION DURING COPPER DEFICIENCY IN RATS

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

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 4/14/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Dietary copper deficiency depresses platelet adhesion and thrombus formation. In the current study, the role of shear rate in in vivo platelet thrombus formation was studied in the cremaster muscle microcirculation of copper-deficient rats. Male, weanling Sprague-Dawley rats were fed purified diets which were either copper-adequate (CuA, 6.3 ug Cu/G diet) or copper-deficient (CuD, 0.3 ug Cu/g diet) for 4 weeks. 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 within the vasculature. In vivo television microscopy was used to quantify thrombus formation. The rate of vessel occlusion caused by thrombus formation was studied at high (277 +/- 31 s**-1) and low (134 +/- 19 s**-1) wall shear rates in third order venules. The low shear rate was achieved by partial manual restriction of the appropriate second order venule. In CuD rats the time to platelet occlusion was significantly longer than for CuA rats at both shear rates. However, the occlusion rate for CuD rats, stated as a percentage of that for CuA rats, was the same for high (41 +/- 18%) and low (44 +/ 8%) shear rates. These results indicate that altered shear rate does not account for the depressed in vivo platelet thrombus formation during copper deficiency and that alteration of platelet and endothelial cell properties by copper deficiency may be of greater importance than rheological factors in delaying thrombosis.