Skip to main content
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 #71390
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: Proceedings
Publication Acceptance Date: 5/19/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Dietary copper deficiency has been shown to alter inflammatory responses and dilation of blood vessels. Endotoxin is a component of bacteria which, if it enters the blood stream, initiates inflammation. The purpose of this study was to examine the effect of copper deficiency on a component of endotoxin-induced inflammation, the dilatory response of small blood vessels. This effect was determined by microscopic observation of the cremaster muscle microcirculation of rats. Injection of endotoxin into the veins of copper-deficient rats caused a relatively greater dilation of small blood vessels than it did in copper-adequate rats. Chemical blockade of the pathways of two potential molecular mediators of endotoxin action, nitric oxide and prostaglandin, indicated that the enhanced dilatory response in copper-deficient rats is caused by an increase in production of or sensitivity to a prostaglandin, perhaps prostacyclin. This information will be useful to scientists and consumers interested in trace element nutrition of the cardiovascular system.

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 induced by lipopolysaccharide (LPS) during dietary copper restriction. Male, weanling Sprague-Dawley rats were fed purified diets that 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 (2.10**-4M) or cyclooxygenase inhibitor ibuprofen (9.6x10**-5M). Vessel diameters were measured every 15 min for 2 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 These results suggest that dietary copper deficiency increases the arteriolar dilation response to LPS. The mechanism apparently involves an increased response to arachidonic acid metabolites but not to NO. Supported by USDA Agreement 95-37200-1625.