EXPERIMENTAL IRON-DEFICIENCY IN RATS - MECHANICAL AND ELECTROPHYSIOLOGICAL ALTERATIONS IN THE CARDIAC-MUSCLE

1. Our aim was to investigate the effect of experimental iron deficien cy on cardiac functional properties. We recorded ventricular isometric twitch, action potentials and the L-type Ca2+ current in isolated ven tricular myocytes from iron-deficient rats and control rats. 2. Twitch tension and maximal rates of tension activation and relaxation were r educed in iron-deficient compared with control rats, whereas twitch du ration was prolonged. Isoproterenol (10(-6) mol/l) augmented tension i n iron-deficient rats (P<0.05), but only moderately affected control r ats. In contrast, maximal rates of tension activation and relaxation w ere increased equally by isoproterenol in the two groups. 3. To determ ine the mechanism(s) responsible for the reduced mechanical function i n iron-deficient rats, action potentials and the L-type Ca2+ current ( with or without isoproterenol) were recorded in both groups. 4. The L- type Ca2+ current was smaller in ventricular myocytes from control rat s than in those from iron-deficient rats; at a membrane potential of 0 mV, L-type Ca2+ current amplitudes were -1.44+/-0.18 and -0.97+/-0.07 nA in myocytes from control and iron-deficient rats respectively (P<0 .05). 5. Action potential duration was markedly shortened in myocytes from iron-deficient compared with control rats; action potential durat ion at 50% repolarization was 12.0+/-1.6 and 7.2+/-1.4 ms in myocytes from control and iron-deficient rats respectively (P<0.01). These iron deficiency-induced electrophysiological alterations most probably con tribute to the depressed mechanical function in iron-deficient rats. 6 . The L-type Ca2+ current was augmented equally by isoproterenol in th e two groups, suggesting that the enhanced inotropic responsiveness in iron-deficient rats was not due to an increased response of the L-typ e Ca2+ current. 7. These results may have an important implication for anaemic (iron-deficient) patients; the attenuation of their cardiac m echanical performance may be compensated by an increased reactivity to beta-adrenergic stimulation.