Nerve agents (NAs) are potent organophosphorus (OP) compounds with applications in chemical warfare. OP compounds act by inhibiting acetylcholinesterase (AChE). Soman (O-pinacolyl methylphosphonofluoridate) is one of the most potent NAs. It is well known that small doses of NAs can be lethal, and that even non-lethal exposure leads to long-term mental debilitation/neurological damage. However, the neuropathology following exposure to sub-lethal nerve agents is not well understood.

In this study, we examined changes in tissue oxygenation (pO₂) in the cortex and hippocampus after a sub-lethal dose of soman [80–90 μg/kg; subcutaneous]. pO₂ changes can provide information regarding oxygen delivery and utilization and may be indicative of a disruption in cerebral blood flow and/or metabolism. Changes in oxygenation were measured with chronically implanted oxygen sensors in awake and freely moving rats. Measurements were taken before, during, and after soman-induced convulsive seizures.

Soman exposure resulted in an immediate increase in pO₂ in the cortex, followed by an even greater increase that precedes the onset of soman-induced convulsive seizures. The rise in hippocampus pO₂ was delayed relative to the cortex, although the general pattern of brain oxygenation between these two regions was similar. After convulsive seizures began, pO₂ levels declined but usually remained hyperoxygenated. Following the decline in pO₂, low frequency cycles of large amplitude changes were observed in both the cortex and hippocampus. This pattern is consistent with recurring seizures.

Measuring real-time changes in brain pO₂ provides new information on the physiological status of the brain following soman exposure. These results highlight that the measurement of brain oxygenation could provide a sensitive marker of nerve agent exposure and serve as a biomarker for treatment studies.

神经剂（NAs）是有效的有机磷（OP）化合物，可用于化学战。OP化合物通过抑制乙酰胆碱酯酶（AChE）发挥作用。梭曼（O-频哪醇甲基氟膦酸酯）是最有效的NAs之一。众所周知，小剂量的NAs可能致命，甚至非致命性暴露也会导致长期的精神衰弱/神经系统损害。但是，接触致死性神经毒剂后的神经病理学还不清楚。

在这项研究中，我们研究了亚致死剂量的梭曼[80–90μg/ kg；皮下注射]后皮层和海马组织氧合（pO ₂）的变化。皮下]。pO _2的变化可以提供有关氧的输送和利用的信息，并且可以指示脑血流和/或新陈代谢的破坏。用清醒和自由运动的大鼠中长期植入的氧传感器测量氧合作用的变化。在梭曼诱发的抽搐发作之前，之中和之后进行测量。

Soman暴露导致皮质中pO ₂立即增加，随后在soman诱发的抽搐性发作发作之前出现更大的增加。尽管这两个区域之间的脑氧合基本模式相似，但海马pO ₂的升高相对于皮质延迟了。抽搐发作开始后，pO ₂含量下降，但通常保持高氧状态。随着pO ₂的下降，在皮层和海马体均观察到大幅度变化的低频周期。这种模式与反复发作有关。

测量人脑中pO ₂的实时变化可提供有关人暴露于人后大脑的生理状态的新信息。这些结果表明，脑氧合的测量可以提供神经毒剂暴露的敏感标志物，并可以作为治疗研究的生物标志物。