Lawrence C B, Farquharson C
Rowett Research Institute, Bucksburn, Aberdeen, Scotland.
Proc Soc Exp Biol Med. 1988 Nov;189(2):173-82. doi: 10.3181/00379727-189-42794.
Copper (Cu) deficiency, induced in rats by suckling from Cu-deficient dams and by offering a semisynthetic low-Cu diet from weaning, resulted in cardiac enlargement. This enlargement was not due to accumulation of excess fluid in the heart but was characterized by mitochondrial hypertrophy as demonstrated by electron microscopy and biochemical studies. Administration of reserpine limited the extent of cardiac enlargement; however, heart total noradrenaline (NA), unchanged by Cu deficiency, was significantly reduced by reserpine. It was concluded that cardiac enlargement in Cu deficiency was not directly related to NA concentration. An alteration in cardiac energy status, however, was suggested by reduction in activity of the nonheme iron-dependent enzyme, succinic dehydrogenase.
通过让大鼠吸食缺铜母鼠的乳汁以及从断奶后开始提供半合成低铜饮食诱导大鼠缺铜,结果导致心脏增大。这种增大并非由于心脏中过多液体的蓄积,而是以线粒体肥大特征,这一点通过电子显微镜和生化研究得以证实。给予利血平限制了心脏增大的程度;然而,心脏总去甲肾上腺素(NA)虽不受缺铜影响,但利血平使其显著降低。得出的结论是,缺铜时心脏增大与NA浓度无直接关系。不过,非血红素铁依赖性酶琥珀酸脱氢酶活性的降低提示心脏能量状态发生了改变。