Chang F C, Foster R E, Beers E T, Rickett D L, Filbert M G
U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Maryland 21010-5425.
Toxicol Appl Pharmacol. 1990 Feb;102(2):233-50. doi: 10.1016/0041-008x(90)90023-n.
Soman-induced respiratory failure was investigated in awake, behaving guinea pigs chronically instrumented to allow concurrent recordings of medullary respiratory-related unit (RRU) activity, diaphragm electromyogram (DEMG), and electrocorticogram. Responses to soman typically began with hyperpnea. Loss of consciousness, as indicated by the development of seizure activities, took place shortly after the onset of hyperpnea. This was followed by dyspnea, hypopnea, and finally, respiratory failure. The most profound respiratory dysfunctions were seen during the development of dyspnea characterized by a progressively degenerative RRU-DEMG phase relationship (phase anomalies) and mixed patterns of ataxic breathing. Electrophysiographic records indicated that the anomalous RRU-DEMG phase phenomenon is attributable to a state of functional dissociation in some brainstem mechanisms that are normally involved in the orchestration of a synchronous respiratory drive. The failure of bulbar rhythmogenic mechanisms to maintain an orderly and synchronous recruitment of respiratory drive, which led to untimely and chaotic activations of respiratory muscles, was apparently the underlying cause of various ataxic breathing patterns and a reduced ventilatory efficiency. Spectral analyses of DEMG activities showed that, despite episodic muscle fasciculations and signs of fatigue, the functional integrity of the diaphragm was not significantly compromised by soman at a dose sufficient to produce respiratory failure. These findings not only support the notion of a relatively more important involvement of central respiratory mechanisms in soman-induced respiratory failure, but also identify a state of functional dissociation of central respiratory timing mechanisms as being a significant component in soman intoxication.
在清醒、行为正常且长期植入仪器的豚鼠身上研究了梭曼诱导的呼吸衰竭，该仪器可同时记录延髓呼吸相关单位（RRU）活动、膈肌肌电图（DEMG）和脑电图。对梭曼的反应通常始于呼吸急促。如癫痫活动的出现所示，意识丧失在呼吸急促开始后不久发生。随后是呼吸困难、呼吸浅慢，最终发展为呼吸衰竭。在呼吸困难发展过程中观察到最严重的呼吸功能障碍，其特征为RRU-DEMG相位关系逐渐退化（相位异常）和共济失调呼吸的混合模式。电生理记录表明，异常的RRU-DEMG相位现象可归因于一些脑干机制的功能解离状态，这些机制通常参与同步呼吸驱动的协调。延髓节律发生机制无法维持有序和同步的呼吸驱动募集，导致呼吸肌过早和混乱的激活，这显然是各种共济失调呼吸模式和通气效率降低的根本原因。对DEMG活动的频谱分析表明，尽管存在间歇性肌肉束颤和疲劳迹象，但在足以导致呼吸衰竭的剂量下，梭曼并未显著损害膈肌的功能完整性。这些发现不仅支持了中枢呼吸机制在梭曼诱导的呼吸衰竭中相对更重要的参与这一观点，还确定了中枢呼吸定时机制的功能解离状态是梭曼中毒的一个重要组成部分。
