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

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 Fe^(2+)(100 μmol/L, 200 μmol/L) on the left ventricular outflow tract autorhythmic cells.Heart tissues were perfused with FeSO_4(200 μmol/L) combing with CaCl_2(4.2 mmol/L), Verapamil,(1 μmol/L), and nickel chloride(200μmol/L) respectively to observe the influences of these contents on electrophysiology of FeSO_4(200μmol/L) on the left ventricular outflow tract autorhythmic cells.Results: Fe^(2+)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 concentrationdependent manner resulting into decrease in Vmax, APA and MDP, slower RPF and VDD, and prolonged APD_(50) and APD_(90)(P all <0.05).Besides, perfusion of increased Ca^(2+) concentration could partially offset the electrophysiological effects of Fe^(2+)(200 μmol/L).The L-type calcium channel(LTCC) blocker Verapamil(1 μmol/L) could block the electrophysiological effects of Fe^(2+)(200 μmol/L).But the T-type calcium channel(TTCC) blocker nickel chloride(NiCl_2, 200 μmol/L) could not block the electrophysiological effects of Fe^(2+)(200 μmol/L).Conclusions: Fe^(2+) 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.

Effects of hydrogen sulfide on guinea pig aortic vestibule autorhythmic cells electrophysiology and its mechanism

Objective:To investigate the electrophysiological effects of hydrogen sulfide (H2S) on left ventricular outflow tract autonomic cells in guinea pigs and its mechanism.Methods:Intracellular microelectrode recording technique was used to observe the electrophysiological effects of different concentrations of hydrogen sulfide on the autonomic cells of left ventricular outflow tract.Results: CSE irreversible inhibitor PPG (200 μmol/L) makes the left ventricular outflow tract of autorhythmic cells Vmax, RPF and VDD accelerate, APA increase (P<0.05);CBS synthase inhibitor AOAA (100μmol/L) acts on the autorhythmic cells of the left ventricular outflow tract without effect. The concentration-dependency of the 50, 100 and 200μmol/L NaHS made RPF and VDD of autorhythmic cell of the left ventricular outflow tract decrease with increasing concentration of NaHS, Vmax and APA decrease (P<0.01). The ATP sensitive potassium channel (KATP) blocker glybenclamide (Gli, 20 μmol/L) partially blocked the electrophysiological effects of NaHS (P<0.05). The L-Ca2+ channel agonist Bay K8644 could partially block the electrophysiological effects of NaHS.Conclusion:The autorhythmic cells of the left ventricular outflow tract had endogenous H2S produced by CSE. H2S had a negative chronotropic effect on autorhythmic cells in the left ventricular outflow tract, and its mechanism was related to the inhibition of L-Ca2+ channels by the open KATP pathway.