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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #67293
Title: COPPER DEFICIENCY INCREASES MICROVASCULAR DILATION TO ENDOTOXIN

Author
item SCHUSCHKE, DALE - U LOUISVILLE
item Saari, Jack
item MILLER, FREDERICK - U LOUISVILLE

Submitted to: Trace Elements in Man and Animals International Symposium
Publication Type: Abstract Only
Publication Acceptance Date: 5/19/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: We have previously reported that there is an altered response to mast cell-mediated inflammation in copper-deficient rats. In the current study we determined the microvascular reactivity to inflammatory stimuli with lipopolysaccharide (LPS) during dietary copper restriction. Male, weanling Sprague-Dawley rats were fed purified diets which were either copper-adequate (CuA, 6 ug Cu/g) or copper-deficient (CuD, 0 ug/g) for 4 weeks. Rats were anesthetized and the cremaster muscle was prepared for in vivo television microscopy. Arteriolar diameters were measured and then 2.5 mg/kg LPS was injected i.p. In separate groups animals were pretreated with the NO-synthase inhibitor L-NAME (2x10**-4 M) or cyclooxygenase inhibitor ibuprofen (9.6x10**-5 M). Vessel diameters were measured every 15 min for two hours and the maximal diameters in um+/-SEM are presented in the table. Baseline LPS (ET) LPS+L-NAME LPS+Ibuprofen CuA 13.2+/-1.0 19.2+/-1.0 24.2+/-2.3**b 13.6+/-1.3**b CuD 13.2+/-1.0 26.4+/-2.5**a 27.6+/-2.2 18.4+/-1.3**a,b **a p<0.05 compared to CuA value; **b p<0.05 compared to LPS alone These results suggest that dietary copper deficiency increases the arteriolar dilation to LPS. The mechanism appears to involve a greater response to arachidonic acid metabolites but not NO. Supported by USDA agreement 95-37200-1625.