Leukocyte–endothelial adhesion is impaired in the cremaster muscle microcirculation of the copper-deficient rat

Abstract

Dietary copper deficiency impairs the function of both the vascular endothelium and circulating leukocytes. In the current study, leukocyte–endothelium adhesion was observed in the in vivo cremaster muscle microcirculation of copper-adequate and copper-deficient rats. Male, weanling Sprague–Dawley rats were fed purified diets that were either adequate (5.6 μg/g) or deficient (0.3 μg/g) in copper. Adhesion was stimulated with the inflammatory mediators tumor necrosis factor-α and bradykinin, and the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine. Intravascular adhesion of leukocytes to the vascular endothelium was significantly attenuated in the copper-deficient group in response to all three agonists. These results occurred without any difference in intravascular wall shear rate between the dietary groups. Based on previous work, we propose that the attenuated response is caused by either decreased expression of adhesion molecules on leukocytes and endothelial cells or by inhibition of the endothelial cell calcium signaling associated with copper deficiency.