Pfister H W, Koedel U, Dirnagl U, Haberl R L, Feiden W, Einhäupl K M
Department of Neurology, University of Munich, Federal Republic of Germany.
Acta Neurochir Suppl (Wien). 1990;51:378-80. doi: 10.1007/978-3-7091-9115-6_127.
The purpose of this study was to identify mediators of brain oedema formation in experimental pneumococcal meningitis. In a rat model of pneumococcal meningitis brain water content was significantly elevated 6 hours post infection (79.69% +/- 0.24 compared to 78.94% +/- 0.16 in the control group, mean +/- SEM, p less than 0.05). Brain oedema formation was completely blocked by superoxide dismutase (132,000 U/kg i.v. per 6 hours: n = 6), pretreatment with dexamethasone (3 mg/kg i.p., n = 3), or administration of dexamethasone at two hours after pneumococcal injection (n = 5). Pretreatment with indomethacin (10 mg/kg i.v., n = 5) attenuated the brain oedema formation. These findings suggest that oxygen derived free radicals act as mediators of brain oedema formation during the early phase of experimental bacterial meningitis. Cyclooxygenase metabolites may provide one possible source for the generation of oxygen derived free radicals in bacterial meningitis.
本研究的目的是确定实验性肺炎球菌性脑膜炎中脑水肿形成的介质。在肺炎球菌性脑膜炎大鼠模型中，感染后6小时脑含水量显著升高（79.69%±0.24，而对照组为78.94%±0.16，均值±标准误，p<0.05）。超氧化物歧化酶（每6小时静脉注射132,000 U/kg：n = 6）、地塞米松预处理（腹腔注射3 mg/kg，n = 3）或肺炎球菌注射后两小时给予地塞米松（n = 5）可完全阻止脑水肿形成。吲哚美辛预处理（静脉注射10 mg/kg，n = 5）可减轻脑水肿形成。这些发现表明，氧衍生自由基在实验性细菌性脑膜炎早期作为脑水肿形成的介质起作用。环氧化酶代谢产物可能是细菌性脑膜炎中氧衍生自由基产生的一个可能来源。
