Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang, Hebei 050017, China.
Chin Med J (Engl). 2011 Nov;124(21):3455-9.
It has been reported that endogenous or exogenous hydrogen sulfide (H(2)S) exerts physiological effects in the vertebrate cardiovascular system. We have also demonstrated that H(2)S 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 H(2)S on human atrial fibers.
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.
NaHS (H(2)S donor) (50, 100 and 200 µmol/L) decreased the amplitude of action potential (APA), maximal rate of depolarization (V(max)), velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF), and shortened the duration of 90% repolarization (APD(90)) in a concentration-dependent manner. ATP-sensitive K(+) (K(ATP)) channel blocker glibenclamide (Gli, 20 µmol/L) partially blocked the effects of NaHS (100 µmol/L) on human atrial fiber cells. The L-type Ca(2+) channel agonist Bay K8644 (0.5 µmol/L) also partially blocked the effects of NaHS (100 µmol/L). An inhibitor of cystathionine γ-lyase (CSE), DL-propargylglycine (PPG, 200 µmol/L), increased APA, V(max), VDD and RPF, and prolonged APD(90).
H(2)S 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 K(ATP) channels and a concomitant decrease in calcium influx. Endogenous H(2)S may be generated by CSE and act as an important regulator of electrophysiological properties in human atrial fibers.
已有报道称，内源性或外源性的硫化氢（H₂S）在脊椎动物心血管系统中发挥生理作用。我们还证明 H₂S 作为一种重要的调节剂，可调节豚鼠乳头肌的电生理特性以及兔窦房结起搏细胞的电生理特性。本研究旨在观察 H₂S 对人心房纤维的电生理效应。
在心脏手术过程中收集人心房样本。使用标准的细胞内微电极技术记录人心房特化纤维的动作电位参数。
NaHS（H₂S 供体）（50、100 和 200μmol/L）浓度依赖性地降低动作电位幅度（APA）、最大去极化速率（Vmax）、舒张期（相 4）去极化速度（VDD）和起搏频率（RPF），并缩短 90%复极时程（APD90）。ATP 敏感性钾（KATP）通道阻滞剂格列本脲（Gli，20μmol/L）部分阻断了 NaHS（100μmol/L）对人心房纤维细胞的作用。L 型钙（Ca²⁺）通道激动剂 Bay K8644（0.5μmol/L）也部分阻断了 NaHS（100μmol/L）的作用。胱硫醚γ-裂解酶（CSE）抑制剂 DL-丙炔基甘氨酸（PPG，200μmol/L）增加 APA、Vmax、VDD 和 RPF，并延长 APD90。
H₂S 发挥负性变时作用，加速人心房特化纤维的复极，这可能是由于 KATP 通道开放导致钾外流增加，同时钙内流减少所致。内源性 H₂S 可能由 CSE 产生，并作为人心房纤维电生理特性的重要调节因子。
