Pennsylvania State University, College of Medicine, Division of Pulmonary and Critical Care Medicine, Penn State Hershey Medical Center, 500 University Dr., Hershey, PA, USA.
Respir Physiol Neurobiol. 2012 Nov 15;184(2):170-7. doi: 10.1016/j.resp.2012.05.002. Epub 2012 May 9.
Acute H(2)S intoxication produces an increase in ventilation followed by a fatal central apnea. The sites of mediation of H(2)S induced hyperpnea and apnea have been investigated since the early 20th century in various animal models. Hyperpnea is mediated by the arterial chemoreceptors, an effect that can be reproduced by injecting a solution of H(2)S at very high concentrations (high millimolar range), while the fatal apnea, which typically occurs above 1000 ppm in humans, appears to result from the cessation of the activity of the medullary respiratory neurons. More recently, moderate levels of exogenous H(2)S (20-80 ppm) have been shown to reduce, within minutes, the metabolic rate, akin to hypoxia-induced hypometabolism. This response appears to be specific to small sized mammals. The pathway through which low levels of inhaled H(2)S could exert such a powerful effect may be very relevant to the physiological mechanisms controlling non-ATP "metabolic" production. Finally, endogenous H(2)S, produced from cysteine, has been proposed to transduce the effects of hypoxia in the carotid bodies. H(2)S remains a mysterious gas: it is labile, difficult/impossible to properly measure in vivo, its oxidation can take place in most tissues including the blood, and it can affect multiple cellular pathways. The demarcation between effects reflecting a putative physiological function and those related to H(2)S poisoning remains however to be established.
急性 H(2)S 中毒会导致通气增加，随后出现致命的中枢性呼吸暂停。自 20 世纪初以来，人们一直在各种动物模型中研究 H(2)S 诱导通气过度和呼吸暂停的调节部位。通气过度是由动脉化学感受器介导的，这种效应可以通过注射高浓度（高毫摩尔范围）的 H(2)S 溶液来复制，而致命的呼吸暂停通常发生在人类 1000 ppm 以上，似乎是由于延髓呼吸神经元活动停止所致。最近，研究表明，中等水平的外源性 H(2)S（20-80 ppm）可在数分钟内降低代谢率，类似于缺氧诱导的低代谢。这种反应似乎是小型哺乳动物所特有的。吸入的低水平 H(2)S 如何通过特定途径产生如此强大的效应，可能与控制非 ATP“代谢”产生的生理机制非常相关。最后，来自半胱氨酸的内源性 H(2)S 被提出可在颈动脉体中转导缺氧的效应。H(2)S 仍然是一种神秘的气体：它不稳定，在体内难以/不可能正确测量，其氧化可以发生在包括血液在内的大多数组织中，并且可以影响多种细胞途径。但是，反映假定的生理功能的作用与与 H(2)S 中毒相关的作用之间的界限仍有待确定。
