Submitted to: Journal of Trace Elements in Medicine and Biology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 10/29/1998
Publication Date: N/A
Citation: Interpretive Summary: Severe dietary copper deficiency in laboratory animals causes heart enlargement. The cause of this enlargement is not well understood. One hypothesis is that the anemia that often accompanies severe copper deficiency causes the heart to work harder in order to deliver oxygen to tissues. The increase in tension, stretch and energy requirement in the heart caused by this increased work load are known to stimulate heart growth. To test whether anemia may contribute to heart enlargement, we measured heart output, heart rate and blood pressure in copper-deficient and copper-adequate rats. These measurements allowed calculation of total peripheral resistance, an estimate of the resistance to blood flow in the arterial circulation, and stroke volume, the volume of blood ejected in one heart beat. Copper deficiency caused a reduction in total peripheral resistance, an occurrence consistent with anemia. A reduction in total peripheral resistance would be expected to increase the pressure of blood entering the heart causing stretch of the heart wall. Observation of an increase in stroke volume with copper deficiency supports this conclusion. From these findings we conclude that anemia can contribute to the heart enlargement of copper deficiency. This information will be useful to scientists and consumers interested in the role of trace element nutrition on the function of the cardiovascular system.
Technical Abstract: Dietary copper deficiency in animals is often associated with cardiac enlargement and anemia. In this study we examined the hypothesis that anemia leads to a high cardiac output state that results in work induced (physiological) cardiac hypertophy. 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. Although cardiac output was unaffected by dietary copper deficiency, the components of cardiac output were found to vary reciprocally, heart rate decreasing and stroke volume increasing with copper deficiency. Further, total peripheral resistance, calculated as the ratio of mean arterial blood pressure and cardiac output, was depressed by dietary copper deficiency. We conclude that bradycardia and depression of vascular resistance induced d by copper deficiency contribute to increased venous filling and a resultant increase in stroke volume; these factors may lead to cardiac hypertrophy. A significant correlation between stroke volume and heart weight in rats of varying copper status supports this conclusion.