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Platelet thrombus formation and hemostasis are delayed in the microcirculation of copper-deficient rats

Schuschke, Dale A., Saari, Jack T., Nuss, James W., Miller, Frederick N.
Journal of nutrition 1994 v.124 no.8 pp. 1258
copper, nutrient deficiencies, dietary minerals, hemostasis, blood coagulation, nutritional adequacy, heart rate, blood pressure, liver, blood plasma, thromboplastin, prothrombin, arteries, rats, blood platelets, hematocrit
The role of dietary copper in platelet thrombus formation and hemostasis was studied in the cremaster muscle microcirculation. Male weanling Sprague-Dawley rats were fed purified diets that were either copper-adequate (94 micromole Cu/kg diet) or copper-deficient (0 micromole Cu/kg diet) for 1, 3 or 5 wk. The rats were anesthetized with pentobarbital, and the cremaster was spread in a Krebs-filled tissue bath. Fluorescein isothiocyanate tagged to bovine serum albumin (FITC-BSA) was injected intra-arterially. After a 20-min equilibration, blue light (1.8 W/cm2, 450-490 nm) was used to activate the FITC-BSA and induce platelet thrombus formation within the vasculature. In vivo television microscopy was used to quantify the thrombus formation. In rats fed the copper-deficient diet for 3 or 5 wk, platelet thrombus formation induced by photoactivation was significantly (P < 0.05) delayed and prothrombin time was significantly longer but the number of circulating platelets was significantly greater than in age-matched rats fed the copper-adequate diet. Bleeding time, measured after micropuncture of a second-order venule, was significantly longer but hematocrit was significantly lower in rats fed the copper-deficient diet than in those fed the copper-adequate diet. The results demonstrate that platelet-mediated hemostasis is depressed in dietary copper deficiency and that this may be due to a decrease in hematocrit, a decrease in the activity of a coagulation factor and/or an alteration of platelet function.