Submitted to: Nutrition International Congress Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 7/27/1997
Publication Date: N/A
Citation: Interpretive Summary:
Technical Abstract: Contractile function is depressed in hearts of copper-deficient rats. Recent studies have shown that nitric oxide, via stimulation of cyclic GMP (cGMP) production, can impair cardiac contraction. In this study we have examined the possibility that cardiac nitric oxide and, along with it, cGMP production are altered, which would provide a possible explanation for reduced contractile force in copper-deficient animals. Male, weanlin Sprague-Dawley rats were fed diets that were either copper-adequate (CuAd, 6 ug Cu/g diet) or copper-deficient (CuDef, <0.5 ug Cu/g diet) for five weeks. Rats were anesthetized, blood was drawn, and hearts and livers collected. Copper deficiency was confirmed by depressed organ copper concentration, the presence of anemia and enlarged hearts. Nitrate/nitrite concentrations (NOx), measured by HPLC, were elevated in hearts of copper-deficient rats. Cyclic GMP, measured by an enzyme immunoassay method, was elevated in hearts of copper-deficient rats. These findings suggest that nitric oxide and cGMP could contribute to the depressed cardiac contraction found in copper deficiency. However, a direct correlation between nitric oxide/cGMP and force of contraction is needed before this may be stated conclusively. Also, additional study is necessary to determine the cause of the elevated concentrations of nitric oxide/cGMP in copper-deficient hearts. Diet Liver Cu Hct Heart wt Heart Nox Heart cGMP ug/g ug/g % mg/g ug/g ng/g CuAd 12.2 +/- 1.1 40.5 +/- 1.4 3.3 +/- 0.2 3.7 +/- 3.3 9.6 +/- 3.1 CuDef 1.1 +/- 0.2 26.8 +/- 5.3 4.3 +/- 0.6 8.4 +/- 4.4 16.3 +/- 6.3 All CuDef values are different from CuAd values (p<0.05).