磁控下循环铁颗粒致耳蜗缺血:突发性听力损失动物模型。

The American journal of otology Pub Date : 2000-09-01
J M Schweinfurth, A T Cacace
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引用次数: 0

摘要

目的:利用动物模型,将突发性听力损失(SHL)中观察到的失真产物耳声发射的缺失与可能的血栓栓塞性血管原因联系起来。背景:畸变产物耳声发射(dpoae)对耳蜗疾病很敏感,在耳蜗损伤中不存在。在之前的一项研究中,作者表明,75%没有可测量排放物的SHL患者无法恢复听力。排放损失的根本原因尚不清楚,但它可能继发于耳蜗缺血。方法:采用磁控循环铁颗粒对6只新西兰大白兔进行单侧耳蜗栓塞术。通过实验耳和对照耳的DPOAE记录监测耳蜗功能。结果:在所有动物中,排放迅速下降,在栓塞后2小时至3周内波动但恢复到基线,没有留下可测量的残留缺陷。在注入铁溶液和放置磁体10分钟内,dpoae被抑制了5 ~ 19 dB。在30分钟和120分钟时达到最低排放,比栓塞前水平低12至37分贝。2只动物在1至3周时恢复到基线DPOAE水平,没有可识别的残余缺陷。结论:本研究中所见的排放物损失可能与耳蜗缺血有关。兔耳蜗栓塞后dpoae的早期抑制可能与SHL患者无dpoae的早期抑制相似。
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Cochlear ischemia induced by circulating iron particles under magnetic control: an animal model for sudden hearing loss.

Purpose: To correlate the absence of distortion-product otoacoustic emissions observed in sudden hearing loss (SHL) with a possible thromboembolic vascular cause, using an animal model.

Background: Distortion-product otoacoustic emissions (DPOAEs) are sensitive to cochlear disorders and are absent in cochlear injury. In a previous study, the authors showed that 75% of patients with SHL who have no measurable emissions do not recover hearing. The underlying cause of the loss of emissions is unknown, but it may be secondary to cochlear ischemia.

Methods: Six New Zealand white rabbits underwent unilateral cochlear embolization through the use of circulating iron particles under magnetic control. Cochlear function was monitored through DPOAE recordings of the experimental and control ears.

Results: In all animals, a rapid decrease in emissions was noted, which fluctuated but returned to baseline within 2 hours to 3 weeks after embolization, leaving no measurable residual defects. The DPOAEs were suppressed by 5 to 19 dB within 10 minutes of injection of iron solution and magnet placement. The lowest emissions were obtained at 30 minutes and again at 120 minutes, which were 12 to 37 dB below preembolization levels. Two animals returned to baseline DPOAE levels at 1 to 3 weeks, with no identifiable residual deficits.

Conclusion: It is likely that the loss of emissions seen in the present study is related to cochlear ischemia. The early suppression of DPOAEs in the rabbit cochlea after embolization may parallel that in SHL patients with absence of DPOAEs on presentation.

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