硫化氢对家兔窦房结起搏细胞的电生理效应

本研究应用细胞内微电极技术,观察硫化氢(hydrogen sulfide,H2S)对家兔窦房结起搏细胞的电生理效应.结果表明:(1)NaHs(H2S供体)50、100、200 μmol/L浓度依赖地降低家兔窦房结起搏细胞4相去极化速率及起搏放电频率.(2)ATP敏感性钾(ATP-sensitive K ,KATP)通道阻断剂格列苯脲(glybenclamide,Gli,20 μmol/L)阻断NariS(100 μmol/L)的电生理效应.(3)预先应用起搏离子流(pacemaker currenL,If)通道阻断剂氯化铯(CsCl,2 mmol/L)对Naris(100μmol/L.)的电生理效应无影响.(4)胱硫醚-γ裂解酶(cystathionine γ-lyase,CSE)的不可逆抑制剂DL-propargylglycine (PPG,200 μmol/L)的家兔窦房结起搏细胞的动作电位参数无影响.以上结果提示,H2S对家兔窦房结起搏细胞有负性变时作用,这些效应可能与其开放KATP通道,增加K 外流有关,与If无关.本实验没有发现窦房结起搏细胞内有CSE催化产生的内源性H2S的合成.

Electrophysiological effects of hydrogen sulfide on pacemaker cells in sinoatrial nodes of rabbits

The cardiac electrophysiological effects of hydrogen sulfide (H2S) on pacemaker cells in sinoatrial (SA) nodes of rabbits wereexamined using intracellular microelectrode technique. The results obtained were as follows: (1) The velocity of diastolic (phase 4)depolarization (VDD) and rate of pacemaker firing (RPF) in normal pacemaker ceils in SA nodes were decreased by NariS (H2S donor)(50, 100, 200 μmol/L) in a concentration-dependent manner; (2) ATP-sensitive K+(KATP) channel blocker glybenclamide (Gli, 20 μmol/L) blocked the effect of NariS (100 μmol/L) on pacemaker cells; (3) Pretreatment with CsC1 (2 mmol/L), a blocker of pacemaker current(If), did not affect the effect of Naris (100 μmol/L) on SA node pacemaker cells; (4) DL-propargylglycine (PPG, 200 μmol/L), aninhibitor of cystathionine γ-lyase (CSE), did not affect the parameters of action potentials in pacemaker cells in SA nodes. All theseresults suggest that H2S exerts a negative chronotropic action on pacemaker cells in SA nodes of rabbits. These effects are likely due toan increase in potassium efflux through opening KATP channels; Ifis unlikely to play a major role in these effects. In our study, there wasno evidence for the generation of endogenous H2S by CSE in SA node pacemaker cells.