Hemostatic mechanisms in marginally copper-deficient rats.

Severe dietary copper restriction has been shown to alter platelet structure and function and to significantly delay thrombogenesis and hemostasis in rats. In the present study, the relationship between dietary copper status and hemostasis were determined in the rat cremaster muscle microcirculation. Male, weanling Sprague-Dawley rats were fed a purified diet that was made copper-adequate by addition of 6.0 micrograms copper/gm of diet (CuA) or was marginally deficient by adding 1.5 micrograms (CuM1.5) or 3.0 micrograms (CuM3.0) copper/gm of diet for 1, 3, or 5 weeks. The rats were anesthetized with sodium pentobarbital, and the cremaster was spread in a Krebs'-filled tissue bath. Hemostasis was quantified after two methods of thrombus induction: (1) micropuncture of a 60 to 80 microns venule, which exposes subendothelial structures, and (2) intravascular light-dye photochemistry, which does not expose the subendothelial collagen. The CuM1.5 and CuM3.0 diets significantly decreased hepatic copper after 3 weeks as compared with the CuA diet. Bleeding time after micropuncture was significantly longer at all times in the CuM1.5 group and after 5 weeks in the CuM3.0 group. Platelet thrombus formation and time to vessel occlusion in the light dye-treated vessels were not different between any of the dietary groups at any times tested. There was also no difference in prothrombin time (PT), in the activity of copper-related plasma coagulation factors V and VIII, or in the hematocrit between the CuA and CuM1.5 groups.(ABSTRACT TRUNCATED AT 250 WORDS)