Rubio Carmen, Paz Carlos
Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía M.V.S., Insurgentes Sur 3877, 14269 D.F., Mexico, Mexico.
Toxicology. 2003 Sep 30;191(2-3):89-96. doi: 10.1016/s0300-483x(03)00245-2.
Ozone (O(3)) exposure causes pulmonary biochemical changes both in humans and experimental animals, inducing the release of inflammatory mediators such as cytokines and eicosanoids. Some of these reaction products have been characterized as endogenous sleep-promoting substances and have been implicated in the development of sleepiness in patients with inflammatory disease. Furthermore, sleep alterations are known to occur in O(3)-exposed humans and experimental animals. In order to test the probable involvement of such inflammatory mediators in O(3)-induced sleep disorders, we blocked prostaglandin synthesis administrating the cyclooxygenase inhibitor indomethacin (IM) and compared conventional electrographic sleep parameters in rats under four different experimental conditions: treatment with IM alone, O(3)-exposure, pre-treatment with IM plus O(3) exposure, and control conditions. We found that O(3) exposure increased slow wave sleep (SWS) and decreased rapid eye movement sleep (REMs) significantly, while IM pre-treatment reduced these O(3)-induced sleep disorders. IM treatment alone did not affect sleep. These findings strongly support a role for inflammatory mediators in O(3) exposure-induced neurological alterations.
臭氧（O₃）暴露会在人类和实验动物体内引发肺部生化变化，促使细胞因子和类花生酸等炎症介质释放。其中一些反应产物已被鉴定为内源性促睡眠物质，并与炎症性疾病患者的嗜睡症发展有关。此外，已知暴露于臭氧的人类和实验动物会出现睡眠改变。为了测试此类炎症介质可能参与臭氧诱导的睡眠障碍，我们通过给予环氧化酶抑制剂吲哚美辛（IM）来阻断前列腺素合成，并比较了大鼠在四种不同实验条件下的常规脑电图睡眠参数：单独使用IM治疗、臭氧暴露、IM预处理加臭氧暴露以及对照条件。我们发现，臭氧暴露显著增加了慢波睡眠（SWS）并减少了快速眼动睡眠（REMs），而IM预处理减轻了这些由臭氧诱导的睡眠障碍。单独使用IM治疗不影响睡眠。这些发现有力地支持了炎症介质在臭氧暴露诱导的神经改变中所起的作用。
