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ORIGINAL ARTICLE
Year : 2018  |  Volume : 11  |  Issue : 2  |  Page : 151-154

Effect of iron overload on electrophysiology of slow reaction autorhythmic cells of left ventricular outflow tract in guinea pigs


1 Department of haematology, the First Affiliated Hospital of Hebei North University, 075000 Zhangjiakou, Hebei, China
2 Department of Physiology, Basic Medical College, Hebei North University, 075000 Zhangjiakou, Hebei, China
3 Department of Obstetrics and Gynecology, the Sixth Hospital of Zhangjiakou, 075000 Zhangjiakou, Hebei, China

Correspondence Address:
Li-Feng Chen
Department of Physiology, Basic medical college, Hebei North University, 075000 Zhangjiakou, Heibei
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1995-7645.225024

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Objective: To investigate the electrophysiology effects and mechanism of iron overload on the slow response autorhythmic cells in the left ventricular outflow tract of guinea pigs. Methods: Standard microelectrode cell recording techniques were adopted to observe the electrophysiological effects of different concentrations of Fe2+ (100 μmol/L, 200 μmol/L) on the left ventricular outflow tract autorhythmic cells. Heart tissues were perfused with FeSO4 (200 μmol/L) combing with CaC12 (4.2 mmol/L), Verapamil, (1 μmol/L), and nickel chloride (200μmol/L) respectively to observe the influences of these contents on electrophysiology of FeSO4 (200 μmol/L) on the left ventricular outflow tract autorhythmic cells. Results: Fe2+ at both 100 μmol/L and 200 μmol/L could change the electrophysiological parameters of the slow response autorhythmic cells of the left ventricular outflow tract in a concentration-dependent manner resulting into decrease in Vmax, APA and MDP, slower RPF and VDD, and prolonged APD50 and APD90 (P all <0.05). Besides, perfusion of increased Ca2+ concentration could partially offset the electrophysiological effects of Fe2+ (200 μmol/L). The L-type calcium channel (LTCC) blocker Verapamil (1 μmol/L) could block the electrophysiological effects of Fe2+ (200 μmol/L). But the T-type calcium channel (TTCC) blocker nickel chloride (NiCl2, 200 μmol/L) could not block the electrophysiological effects of Fe2+ (200 μmol/L). Conclusions: Fe2+ can directly change the electrophysiological characteristics of the slow response autorhythmic cells of the left ventricular outflow tract probably through the L-type calcium channel.


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