|Stinnett, H - UNIV OF NORTH DAKOTA|
Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: April 6, 1997
Publication Date: N/A
Technical Abstract: Dietary copper deficiency in animals is often associated with cardiac enlargement and anemia. The purpose of this study was to examine the hypothesis that the anemia of copper deficiency leads to high cardiac output that results in work-induced (physiological) cardiac hypertrophy. Blood pressure was measured by carotid cannulation and cardiac output was measured by aortic flow probe in anesthetized, open-chested rats that had been subjected to various degrees of dietary copper deficiency for five weeks. Dietary copper deficiency caused anemia, enlarged hearts and depressed concentrations of copper in heart and liver. Cardiac output was unaffected by dietary copper deficiency. However, the components of cardiac output varied reciprocally, heart rate decreasing and stroke volume increasing with copper deficiency. Further, total peripheral resistance, calculated as the ratio of mean arterial blood pressure to cardiac output, was depressed by dietary copper deficiency. We conclude that copper-deficiency-induced bradycardia and depression of vascular resistance can contribute to increased venous filling and a resultant increase in stroke volume, which may in turn lead to cardiac hypertrophy. A significant correlation (p<0.05) between stroke volume and heart weight in rats of varying copper status supports this conclusion.