Smith Howard S
Albany Medical College, Department of Anesthesiology, Albany, NY 12208, USA.
Pain Physician. 2009 Sep-Oct;12(5):901-10.
Hydrogen sulfide (H2S) is a malodorous gas which functions as an endogenous gasotransmitter in humans. It is becoming appreciated that H2S may be involved in a wide variety of processes including nociceptive processes. The molecular mechanisms responsible for many of the activities of H2S remain uncertain, however, H2S increases cAMP levels in neuronal and glial cell lines and primary neuron cultures with hyperpolarization. H2S may be involved in multiple signaling pathways and produce various effects on ion channels (e.g. T-type calcium channel currents, ATP-sensitive K+ (KATP) channels) which may inhibit or promote nociception. It is also conceivable that H2S may affect the n-methyl-d aspartate (NMDA) receptor complex and/or TRPA1 ion channels which may modulate nociceptive processes. It appears that H2S may regulate key neuronal functions, including the induction of hippocampal long-term potentiation, a synaptic model of learning and memory thought to involve the NMDA receptor as well as the release of corticotrophin-releasing hormone from the hypothalamus. It seems that the primary role of H2S in nociceptive processes is the activation of T-type calcium channels leading to facilitation of pronociceptive processes. A secondary contribution to the facilitation of pronociceptive processes may come from H2S-induced activation. It would appear that much like other gasotransmitters (e.g. nitric oxide), endogenous H2S may be involved in multiple physiologic processes and its effects remain complex, difficult to predict, and may vary depending on the specific environment/circumstances/location where it is generated. A greater understanding of the clinically significant human physiology of H2S and hydrogen sulfide's effects on modulating nociceptive processes may potentially lead to novel targets for improving analgesia.
硫化氢（H₂S）是一种有恶臭的气体，在人体中作为内源性气体递质发挥作用。人们逐渐认识到，H₂S可能参与包括伤害感受过程在内的多种过程。然而，H₂S许多活性所涉及的分子机制仍不明确，H₂S可使神经元和神经胶质细胞系以及原代神经元培养物中的环磷酸腺苷（cAMP）水平升高并伴有超极化。H₂S可能参与多种信号通路，并对离子通道（如T型钙通道电流、ATP敏感性钾（KATP）通道）产生各种影响，这些影响可能抑制或促进伤害感受。还可以想象，H₂S可能影响N-甲基-D-天冬氨酸（NMDA）受体复合物和/或瞬时受体电位锚蛋白1（TRPA1）离子通道，从而调节伤害感受过程。似乎H₂S可能调节关键的神经元功能，包括海马体长期增强效应的诱导，这是一种学习和记忆的突触模型，被认为涉及NMDA受体以及下丘脑促肾上腺皮质激素释放激素的释放。看来H₂S在伤害感受过程中的主要作用是激活T型钙通道，从而促进伤害感受过程。对伤害感受过程促进作用的次要贡献可能来自H₂S诱导的激活。看起来，与其他气体递质（如一氧化氮）非常相似，内源性H₂S可能参与多种生理过程，其作用仍然复杂、难以预测，并且可能因产生它的特定环境/情况/位置而异。对H₂S具有临床意义的人体生理学以及硫化氢对调节伤害感受过程的影响有更深入的了解，可能会为改善镇痛效果带来新的靶点。
