Schuschke D A, Saari J T, Ackermann D M, Miller F N
Department of Physiology, University of Louisville School of Medicine, Kentucky 40292.
Am J Physiol. 1989 Nov;257(5 Pt 2):H1607-12. doi: 10.1152/ajpheart.1989.257.5.H1607.
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.
在这项关于铜缺乏的研究中，大鼠肠系膜微循环被用作内源性组胺释放和血小板血栓形成的模型。在实验前，将雄性斯普拉格-道利大鼠分别喂食含铜补充饮食（CuS，5 ppm）或缺铜饮食（CuD，0 ppm）5周。将麻醉大鼠的肠系膜铺展在充满Krebs液的组织浴中。在CuS组动物的小静脉中，与牛血清白蛋白结合的血管内异硫氰酸荧光素的光激活在40分钟时引起显著的血小板聚集和红细胞柱直径（RBCCD）降低，在60分钟时导致血流停滞。在CuD组动物中，只有轻微的血小板聚集，且RBCCD没有降低。血小板聚集测定研究未显示CuD组血小板聚集减少，这表明铜缺乏会改变内皮细胞以抑制黏附。化合物48/80（1.0和10.0微克/毫升）在CuS组和CuD组中均诱导大分子渗漏，且CuD组动物的反应明显更大。结果表明，铜缺乏会导致炎症和血栓形成调节机制的改变。
