Amaee F R, Comis S D, Osborne M P
Department of Physiology, Medical School, University of Birmingham, England.
Acta Otolaryngol. 1995 May;115(3):386-91. doi: 10.3109/00016489509139334.
Sensorineural hearing loss is a major sequela of the bacterial meningitis associated in particular with Streptococcus pneumoniae. Recent studies have shown pneumolysin, a toxin elaborated by S. pneumoniae, to be cytotoxic to the guinea pig cochlea. The mechanisms of this cytotoxicity are, however, not fully understood. In the present study this deleterious action of pneumolysin has been shown to be blocked by pretreating the cochlea with NG-methyl-L-arginine, a known inhibitor of nitric oxide synthesis. Furthermore, pretreatment of the cochlea with MK-801, an NMDA receptor antagonist, was also found to confer marked protection from the action of pneumolysin. This latter finding is consistent with previous reports that excess stimulation of NMDA receptors within the cochlea, an event known to lead to excess nitric oxide release, have similar effects on the cochlea as pneumolysin perfusion. It would therefore appear that nitric oxide may represent a significant link in the chain of events leading to the deafness of bacterial meningitis.
感音神经性听力损失是细菌性脑膜炎的主要后遗症，尤其与肺炎链球菌相关。最近的研究表明，肺炎链球菌产生的毒素——肺炎溶血素对豚鼠耳蜗具有细胞毒性。然而，这种细胞毒性的机制尚未完全了解。在本研究中，已证明用一氧化氮合成的已知抑制剂NG-甲基-L-精氨酸预处理耳蜗可阻断肺炎溶血素的这种有害作用。此外，还发现用NMDA受体拮抗剂MK-801预处理耳蜗可显著保护其免受肺炎溶血素的作用。后一发现与先前的报道一致，即耳蜗内NMDA受体的过度刺激（已知会导致一氧化氮释放过多）对耳蜗的影响与肺炎溶血素灌注相似。因此，一氧化氮可能是导致细菌性脑膜炎耳聋的一系列事件中的重要环节。
