Roos K L
Department of Neurology, Indiana University School of Medicine, Indianapolis.
Clin Ther. 1990 Jul-Aug;12(4):290-6; discussion 289.
It has been shown in experimental models of bacterial meningitis that bacterial cell-wall components produce an inflammatory response in the subarachnoid space, probably by stimulating the release of inflammatory cytokines, such as tumor necrosis factor, interleukin-1, and prostaglandins. Interleukin-1 increases the concentration of prostaglandin E2 and leukotriene B4, metabolites of arachidonic acid, which are potent mediators of inflammation. Steroidal and nonsteroidal anti-inflammatory agents decrease formation of these metabolites and minimize the damage to the blood-brain barrier. There is also evidence that anti-inflammatory agents decrease cerebral edema in bacterial meningitis. The results of clinical trials in patients with bacterial meningitis demonstrate that dexamethasone can prevent sensorineural hearing loss and reduce mortality, without interfering with the antimicrobial action of antibiotics.
在细菌性脑膜炎的实验模型中已表明，细菌细胞壁成分可能通过刺激炎性细胞因子如肿瘤坏死因子、白细胞介素 -1和前列腺素的释放，在蛛网膜下腔产生炎症反应。白细胞介素 -1会增加花生四烯酸的代谢产物前列腺素E2和白三烯B4的浓度，而这些是强力的炎症介质。甾体和非甾体类抗炎药可减少这些代谢产物的形成，并使血脑屏障的损伤最小化。也有证据表明抗炎药可减轻细菌性脑膜炎中的脑水肿。对细菌性脑膜炎患者的临床试验结果表明，地塞米松可预防感音神经性听力损失并降低死亡率，而不会干扰抗生素的抗菌作用。
