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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 #107244
Title: ISOLATED VENTRICULAR MYOCYTES FROM COPPER-DEFICIENT RAT HEARTS EXHIBIT ENHANCED CARDIAC CONTRACTILE FUNCTION

Author
item WOLD, L - UNIV OF NORTH DAKOTA
item Saari, Jack
item REN, J - UNIV OF NORTH DAKOTA

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/10/1999
Publication Date: 3/15/2000
Citation: Wold, L.E., Saari, J.T., Ren, J. 2000. Isolated ventricular myocytes from copper-deficient rat hearts exhibit enhanced cardiac contractile function [abstract]. The Federation of American Societies for Experimental Biology Journal. 14:A157.

Interpretive Summary:

Technical Abstract: Dietary copper deficiency leads to cardiac hypertrophy, cardiac fibrosis, derangement of myofibrils, and impaired cardiac contractile and electrophysiological functioning. However, evidence that copper deficiency affects single cardiac myocyte function has rarely been seen. The purpose of the present study was to determine if the impaired cardiac function in copper deficiency is due to depressed contractile function at the single cell level. Male Sprague-Dawley rats were fed diets that were either copper-adequate (6.3 mg Cu/kg diet) or copper-deficient (0.4 mg Cu/kg diet) for 5 weeks. Ventricular myocytes were dispersed and mechanical properties were evaluated using the SoftEdge video edge- detection system. Myocytes were electrically stimulated to contract at 0.5 Hz. The contractile properties evaluated included peak shortening (PS), time-to-peak shortening (TPS), time-to-90% relengthening (TR90), and maximal velocities of shortening and relengthening (+/-dL/dt). The copper-deficient rats displayed cardiac hypertrophy, hepatomegaly and kidney hypertrophy. Myocytes from the copper-deficient rat hearts exhibited significantly enhanced PS associated with shortened TPS, compared with those from copper-adequate rat hearts. TR90 and +/-dL/dt were not different between the two groups. These data tend to indicate that the impaired contractile function seen in copper-deficient hearts might not be due to depressed cardiac contractile function at the single cell level, but rather due to other mechanisms such as cardiac fibrosis. The enhanced cardiac contractile function may be related to an adaptation response to cardiac hypertrophy, as observed in hypertension.