Böhmer A
Otolaryngologic Clinic, University Hospital, Zürich, Switzerland.
Acta Otolaryngol Suppl. 1993;507:3-24.
The present study summarizes the experimental findings obtained on the pressure in the inner ear fluids and on the effects of pressure changes on cochlear function in the guinea pig. Two types of pressures have to be distinguished in the inner ear fluid compartments: (i) hydrostatic fluid pressure and (ii) superimposed hydrodynamic high frequency (> 100 Hz) sound pressure oscillations. Hydrostatic pressure in the inner ear fluids in guinea pigs is in the order of 200 Pa (2 cm H2O) and shows slow (< 5 Hz) respiratory and pulsatory oscillations as well as considerable physiological variations in the range of -100 to +700 Pa. In normal ears, hydrostatic pressure in the perilymph equals pressure in the endolymph, and pressure changes applied to one compartment are immediately transmitted to the other one. A high compliance of Reissner's membrane seems to be the cause of this endolymphatic-perilymphatic pressure equalization. In experimental endolymphatic hydrops, a unique animal model for Meniere's disease, endolymphatic pressure is higher (100 Pa and above) than perilymphatic pressure. These pressure gradients occur only in late stages of hydrops, probably when Reissner's membrane has lost its high compliance after long standing distension. Positive endolymphatic-perilymphatic pressure gradients are secondary to and not the primary cause of hydrops formation. Changes of hydrostatic pressure do not affect auditory function as long as they stay in the physiological range. This includes the sudden loss of positive inner ear pressure that occurs in perilymph fistulas. The rationale for surgical repair of perilymph fistulas in patients in order to restore the hearing function thus becomes questionable. Other aspects of surgical repair, however, as e.g. prevention of labyrinthitis due to permanently open fistula, could not be investigated in this model, because in guinea pigs even large fistulas heal spontaneously within a few days. In experimental endolymphatic hydrops, deterioration of auditory thresholds was partially correlated to the presence of positive endolymphatic-perilymphatic pressure gradients. A change in pressure, however, occurred later than the first deterioration in auditory function. Therefore positive endo-perilymphatic pressure gradients may contribute to, but are not the only cause of hearing impairment.
本研究总结了在豚鼠内耳液体压力以及压力变化对耳蜗功能影响方面所获得的实验结果。内耳液腔中必须区分两种类型的压力：（i）静水压力和（ii）叠加的流体动力高频（>100Hz）声压振荡。豚鼠内耳液体中的静水压力约为200Pa（2cmH₂O），呈现缓慢（<5Hz）的呼吸和搏动振荡，以及在-100至+700Pa范围内相当大的生理变化。在正常耳中，外淋巴中的静水压力等于内淋巴中的压力，施加于一个腔室的压力变化会立即传递到另一个腔室。Reissner膜的高顺应性似乎是这种内淋巴-外淋巴压力平衡的原因。在实验性内淋巴积水（梅尼埃病的一种独特动物模型）中，内淋巴压力高于外淋巴压力（100Pa及以上）。这些压力梯度仅在积水的后期出现，可能是在Reissner膜因长期扩张而失去其高顺应性之后。内淋巴-外淋巴正压力梯度是积水形成的继发因素而非主要原因。只要静水压力保持在生理范围内，其变化就不会影响听觉功能。这包括外淋巴瘘中出现的内耳正压力突然丧失。因此，为恢复听力功能而对患者进行外淋巴瘘手术修复的理论依据变得值得怀疑。然而，手术修复的其他方面，例如预防因瘘管永久开放导致的迷路炎，在该模型中无法进行研究，因为在豚鼠中，即使是大的瘘管也会在几天内自发愈合。在实验性内淋巴积水中，听觉阈值的恶化部分与内淋巴-外淋巴正压力梯度的存在相关。然而，压力变化发生的时间晚于听觉功能的首次恶化。因此，内淋巴-外淋巴正压力梯度可能导致听力损害，但不是唯一原因。
