AJP - Heart Myographs and Tissue organ baths
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Am J Physiol Heart Circ Physiol 257: H1607-H1612, 1989;
0363-6135/89 $5.00
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AJP - Heart and Circulatory Physiology, Vol 257, Issue 5 1607-H1612, Copyright © 1989 by American Physiological Society

ARTICLES

Microvascular responses in copper-deficient rats

D. A. Schuschke, J. T. Saari, D. M. Ackermann and F. N. Miller
Department of Physiology, University of Louisville School of Medicine, Kentucky 40292.

In this study on copper deficiency, the rat crewmaster microcirculation was used as a model for endogenous histamine release and platelet thrombi formation. Male Sprague-Dawley rats were fed either a copper-supplemented diet (CuS, 5 ppm) or a copper-deficient diet (CuD, 0 ppm) for 5 wk before experimentation. The crewmasters of anesthetized rats were spread in a Krebs-filed tissue bath. In venules of CuS animals, photoactivation of intravascular fluorescein isothiocyanate tagged to bovine serum albumin caused significant platelet aggregation and reduction of red blood cell column diameter (RBCCD) by 40 min and stasis of flow by 60 min. In CuD animals there was only minor platelet aggregation and no reduction in RBCCD. Platelet aggregometry studies did not demonstrate reduced platelet aggregation in the CuD group, suggesting that copper deficiency alters the endothelium to inhibit adhesion. Compound 48/80 (1.0 and 10.0 microgram/ml) induced macromolecular leakage in both CuS and CuD groups, with the response in the CuD animals being significantly greater. The results demonstrate that copper deficiency results in alterations of the regulatory mechanisms governing inflammation and thrombosis.


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J. J. D. Lucca, J. T. Saari, J. C. Falcone, and D. A. Schuschke
Neointima Formation in the Rat Carotid Artery Is Exacerbated by Dietary Copper Deficiency
Experimental Biology and Medicine, July 1, 2002; 227(7): 487 - 491.
[Abstract] [Full Text] [PDF]


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