Isolated ventricular myocytes from copper-deficient rat hearts exhibit enhanced contractile function

Dietary copper deficiency leads to cardiac hypertrophy, cardiac fibrosis, d erangement of myofibrils, and impaired cardiac contractile and electrophysi ological function. The purpose of this study was to determine whether impai red cardiac function from copper deficiency is due to depressed contractile function at the single myocyte level. Male Sprague-Dawley rats were fed di ets that were either copper adequate (5.59-6.05 mug copper/g body wt; n = 1 1) or copper deficient (0.29-0.34 mug copper/g body wt; n = 11) for 5 wk. V entricular myocytes were dispersed and mechanical properties were evaluated using the SoftEdge video-based edge-detection system. Intracellular Ca2+ t ransients were examined using fura 2-acetoxymethyl ester. Myocytes were ele ctrically stimulated to contract at 0.5 Hz. Properties evaluated included p eak shortening (PS), time to peak shortening (TPS), time to 90% relengtheni ng (TR90), and maximal velocities of shortening and relengthening (+/-dL/dt ). Myocytes from the copper-deficient rat hearts exhibited significantly en hanced PS values associated with shortened TR90 measurements compared with those from copper-adequate rat hearts. The +/-dL/dt values were enhanced an d the intracellular Ca2+ transient decay rate was depressed in myocytes fro m copper-deficient rats. These data indicate that impaired cardiac contract ile function that is seen in copper-deficient whole hearts might not be due to depressed cardiac contractile function at the single cell level but rat her to other mechanisms such as cardiac fibrosis.