CAJ | 학술논문

目的在耳毒性损伤的豚鼠模型上诱发声诱发短潜伏期负电位( acoustically evoked short latency negative response,ASNR),通过内耳铺片观察ASNR豚鼠的基底膜球囊、椭圆囊及半规管壶腹的组织形态学特点,验证豚鼠ASNR的责任终器.方法将45只健康豚鼠按随机数字表法分为2组,健康对照组15只(30耳),药物致聋组30只(60耳).致聋组给药(硫酸卡那霉素+利尿酸)致聋7～10d后,行听觉脑干反应(ABR)测试,根据ASNR引出情况进一步分为ASNR组和非ASNR组.三组豚鼠断头取颞骨,解剖显微镜下取出基底膜、球囊斑、椭圆囊斑和壶腹嵴,通过显微镜观察毛细胞数目和形态变化.结果致聋组有27只动物(54耳)完成测试,其中45耳达到重度感音神经性聋,19耳引出ASNR(35.2％),阈值为110～125 dBSPL,平均阈值(121.7±4.5)dBSPL,潜伏期1.80～2.08 ns,平均潜伏期(1.93±0.07)ms.铺片观察显示,基底膜、球囊、随圆囊、壶腹嵴毛细胞密度按正常对照组、ASNR组、非ASNR组依次减低,毛细胞损伤程度依次加重.ASNR组球囊微纹区、周边区毛细胞密度与对照组差异无统计学意义(P值均＞0.05)；其他各组的相应比较,差异均有统计学意义(P值均＜0.05).结论豚鼠ASNR的责任终器是球囊,而不依赖于耳蜗、椭圆囊及半规管功能.
목적 재이독성손상적돈서모형상유발성유발단잠복기부전위( acoustically evoked short latency negative response,ASNR),통과내이포편관찰ASNR돈서적기저막구낭、타원낭급반규관호복적조직형태학특점,험증돈서ASNR적책임종기.방법 장45지건강돈서안수궤수자표법분위2조,건강대조조15지(30이),약물치롱조30지(60이).치롱조급약(류산잡나매소+이뇨산)치롱7～10d후,행은각뇌간반응(ABR)측시,근거ASNR인출정황진일보분위ASNR조화비ASNR조.삼조돈서단두취섭골,해부현미경하취출기저막、구낭반、타원낭반화호복척,통과현미경관찰모세포수목화형태변화.결과 치롱조유27지동물(54이)완성측시,기중45이체도중도감음신경성롱,19이인출ASNR(35.2％),역치위110～125 dBSPL,평균역치(121.7±4.5)dBSPL,잠복기1.80～2.08 ns,평균잠복기(1.93±0.07)ms.포편관찰현시,기저막、구낭、수원낭、호복척모세포밀도안정상대조조、ASNR조、비ASNR조의차감저,모세포손상정도의차가중.ASNR조구낭미문구、주변구모세포밀도여대조조차이무통계학의의(P치균＞0.05)；기타각조적상응비교,차이균유통계학의의(P치균＜0.05).결론 돈서ASNR적책임종기시구낭,이불의뢰우이와、타원낭급반규관공능.
Objective To establish a model of ototoxicity in guinea pigs with acoustically evoked short latency negative response (ASNR) and verify the responsible organ of ASNR based on microscopic characteristics of basal membranes,saccules,utricles and ampulla canalis semicircularis of the inner ear.Methods Total of 45 guinea pigs were employed in the experiment,which were randomly divided into the control group (15 subjects,30 ears) and the deafened group (30 subjects,60 ears). Each animal experienced auditory brainstem response ( ABR ). A quick treatment was employed for deafened group consisting of a subcutaneous injection of kanamycin at a dose of 400 mg/kg followed by jugular vein injection of ethacrynic acid at a dose of 40 mg/kg one hour later.The animals were performed ABR test from 7 to 10 days after the drug administration.The deafened group was further divided into ASNR group and non-ASNR group based on the presence of ASNR.All the guinea pigs were sacrificed after ABR tests.The Corti organ,macula sacculi,macula utriculi and crista ampullaris were observed by light microscope.Results In the deafened group (60 ears),3 subjects died postoperatively,27 subjects (54 ears) provided full data.ASNR was elicited in 19 ears (35.2％,19/54 ),the thresholds of ASNR were from 110 to 125 dBSPL with average of ( 121.7 ±4.5)dBSPL ASNR latency ranges were 1.80-2.08 ms,the average latency of thresholds were ( 1.93 ±0.07) ms.The stretched preparation results:overall hair-cell density of macula saccule,macula utriculi and crista ampullaris decreased in order of normal eontrol group,ASNR group and non-ASNR group.There was no difference between the normal group and ASNR group for cell density of macula saccule.Apart from this,statistical differences were found among other groups.Conclusions The present study evoked ASNR in an olotoxicity guinea pig model which was profound hearing loss with normal saccular function and normal saccular hair cell density.It suggested that ASNR originates from the saccule and have no relation with cochlear,utricle and semicircular canal according to morphological study.