Guo Y, Wu Y, Chen W, Lin J
Department of Otolaryngology, Union Hospital, Fuzhou, China.
J Laryngol Otol. 1994 Apr;108(4):310-3. doi: 10.1017/s0022215100126623.
This study presents animal experiments on endotoxin (lipopolysaccharides: LPS) damage to the inner ear with special reference to the stria vascularis. The experimental group animals (albino guinea pigs) were injected with LPS into the perilymphatic space. Pyrogen-free saline (PFS) was injected into the control group. Strial structural evaluation and hearing tests were carried out before and one, three and five days after treatment. In PFS-treated (control) ears, no significant change was found either in hearing or structure. However, thresholds of N1/P1 were elevated and latencies prolonged in LPS-treated ears. They had severe strial damage mainly to the cellular organelles. The mitochondria became swollen with a disordered, broken, degenerated or absent crest. Secondary lysosomes and autophagosomes increased in number with the presence of medulative inclusions. Na(+)-K(+)-ATPase reactant was obviously diminished. It is concluded that LPS-induced strial ototoxicity produces ion imbalance, causing changes in endolymph composition and energy failure in the organ of Corti and is also responsible for the pathogenesis of inner ear sequelae secondary to otitis media.
本研究进行了关于内毒素(脂多糖:LPS)对内耳损伤的动物实验,特别关注血管纹。实验组动物(白化豚鼠)在鼓阶内注射LPS,对照组注射无热原生理盐水(PFS)。在治疗前以及治疗后1天、3天和5天进行血管纹结构评估和听力测试。在PFS治疗(对照)的耳朵中,听力和结构均未发现明显变化。然而,LPS治疗的耳朵中N1/P1阈值升高,潜伏期延长。它们有严重的血管纹损伤,主要累及细胞器。线粒体肿胀,嵴紊乱、断裂、退化或缺失。次级溶酶体和自噬体数量增加,并存在髓样内含物。Na(+)-K(+)-ATP酶反应物明显减少。结论是,LPS诱导的血管纹耳毒性导致离子失衡,引起内淋巴成分变化和柯蒂器能量衰竭,也是中耳炎继发内耳后遗症发病机制的原因。