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

摘要

Objective: To investigate the electrophysiological effects of hydrogen sulfide (H2S) onleft ventricular outflow tract autonomic cells in guinea pigs and its mechanism. Methods:Intracellular microelectrode recording technique was used to observe the electrophysiologicaleffects of different concentrations of hydrogen sulfide on the autonomic cells of left ventricularoutflow tract. Results: CSE irreversible inhibitor PPG (200 μmol/L) makes the left ventricularoutflow tract of autorhythmic cells Vmax, RPF and VDD accelerate, APA increase (P0.05); CBS synthase inhibitor AOAA (100μmol/L) acts on the autorhythmic cells of the leftventricular 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 tractdecrease with increasing concentration of NaHS, Vmax and APA decrease (P0.01). The ATPsensitive potassium channel (KATP) blocker glybenclamide (Gli, 20 μmol/L) partially blockedthe electrophysiological effects of NaHS (P0.05). The L-Ca2+ channel agonist Bay K8644could partially block the electrophysiological effects of NaHS. Conclusion: The autorhythmiccells of the left ventricular outflow tract had endogenous H2S produced by CSE. H2S had anegative chronotropic effect on autorhythmic cells in the left ventricular outflow tract, and itsmechanism was related to the inhibition of L-Ca2+ channels by the open KATP pathway.