Electrophysiological effects of hydrogen sulfide on human atrial fibers
- Author:
- No author available
- Journal Title:
- Chinese Medical Journal
- Issue:
- 21
- DOI:
- 10.3760/cma.j.issn.0366-6999.2011.21.004
- Key Word:
- electrophysiology;hydrogen sulfide;action potential;heart atrium;cystathionine γ-lyase
Abstract： Background It has been reported that endogenous or exogenous hydrogen sulfide (H2S) exerts physiological effects in the vertebrate cardiovascular system.We have also demonstrated that H2S acts as an important regulator of electrophysiological properties in guinea pig papillary muscles and on pacemaker cells in sinoatrial nodes of rabbits.This study was to observe the electrophysiological effects of H2S on human atrial fibers.Methods Human atrial samples were collected during cardiac surgery.Parameters of action potential in human atrial specialized fibers were recorded using a standard intracellular microelectrode technique.Results NaHS (H2S donor) (50,100 and 200 μmol/L) decreased the amplitude of action potential (APA),maximal rate of depolarization (Vmax),velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF),and shortened the duration of 90％ repolarization (APD90) in a concentration-dependent manner.ATP-sensitive K+ (KATP)channel blocker glibenclamide (Gli,20 μmol/L) partially blocked the effects of NaHS (100 μmol/L) on human atrial fiber cells.The L-type Ca2+ channel agonist Bay K8644 (0.5 μmol/L) also partially blocked the effects of NaHS (100 μmol/L).An inhibitor of cystathionine y-lyase (CSE),DL-propargylglycine (PPG,200 μmol/L),increased APA,Vmax,VDD and RPF,and prolonged APD90.Conclusions H2S exerts a negative chronotropic action and accelerates the repolarization of human atrial specialized fibers,possibly as a result of increases in potassium efflux through the opening of KATP channels and a concomitant decrease in calcium influx.Endogenous H2S may be generated by CSE and act as an important regulator of electrophysiological properties in human atrial fibers.
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