Gastroenterology Research Unit and Division of Gastroenterologic and General Surgery, Rochester, MN 55905, USA.
J Gastrointest Surg. 2011 Jan;15(1):12-22. doi: 10.1007/s11605-010-1306-8. Epub 2010 Nov 17.
This study aims to determine mechanisms of action of the gasotransmitter hydrogen sulfide (H(2)S) on contractile activity in longitudinal muscle of rat ileum.
Ileal longitudinal muscle strips were prepared to measure isometric contractions. Effects of sodium hydrosulfide (NaHS), a donor of H(2)S, were evaluated on spontaneous contractile activity and after enhanced contractile activity with bethanechol. L-cysteine was evaluated as a potential endogenous donor of H(2)S. We evaluated involvement of extrinsic nerves, enteric nervous system, visceral afferent nerves, nitric oxide, and K(ATP)(+) channel and K(Ca)(+) channel activity on the action of H(2)S using non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, L-N(G)-nitro arginine (L-NNA), glibenclamide, and apamin, respectively, as well as electrical field stimulation.
NaHS dose-dependently and reversibly inhibited spontaneous and bethanechol-stimulated contractile activity (p < 0.05). L-cysteine had no inhibitory effect. Non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, L-NNA, glibenclamide, or apamin had no major effect on total contractile activity by NaHS, although both tetrodotoxin and apamin decreased the frequency of bethanechol-enhanced contractile activity (p < 0.05). We could not demonstrate H(2)S release by electrical field stimulation but did show that inhibition of cystathionine β synthase, an endogenous source of H(2)S, augmented the inhibitory effect of low-frequency electrical field stimulation.
H(2)S inhibits contractile activity of ileal longitudinal muscle dose-dependently but not through pathways mediated by the extrinsic or enteric nervous system, visceral afferent nerves, nitric oxide, K(ATP)(+) channels, or K(Ca)(+) channels.
本研究旨在确定气体递质硫化氢（H2S）对大鼠回肠纵行肌收缩活动的作用机制。
制备回肠纵行肌条以测量等长收缩。评估硫氢化钠（NaHS），H2S 的供体，对自发性收缩活动的影响，以及对贝那胆碱增强的收缩活动的影响。L-半胱氨酸被评估为 H2S 的潜在内源性供体。我们使用非肾上腺素能/非胆碱能条件、河豚毒素、辣椒素、L-N（G）-硝基精氨酸（L-NNA）、格列本脲和阿帕米，分别评估了外生神经、肠神经系统、内脏传入神经、一氧化氮和 KATP（+）通道和 KCa（+）通道活性对 H2S 作用的影响。以及电刺激。
NaHS 剂量依赖性和可逆地抑制自发性和贝那胆碱刺激的收缩活动（p<0.05）。L-半胱氨酸没有抑制作用。非肾上腺素能/非胆碱能条件、河豚毒素、辣椒素、L-NNA、格列本脲或阿帕米对 NaHS 的总收缩活性没有主要影响，尽管河豚毒素和阿帕米都降低了贝那胆碱增强的收缩活性的频率（p<0.05）。我们无法证明电刺激释放 H2S，但确实表明抑制胱硫醚β合酶，H2S 的内源性来源，增强了低频电刺激的抑制作用。
H2S 剂量依赖性地抑制回肠纵行肌的收缩活动，但不是通过外生或肠神经系统、内脏传入神经、一氧化氮、KATP（+）通道或 KCa（+）通道介导的途径。
