Changes in CMDP and DPOAE during acute increased inner ear pressure in the guinea pig.

During and after an increase of inner ear pressure, induced by injection of artificial perilymph, the 2f1 - f2 and f2 - f1 distortion products (DPs) in cochlear microphonics (CM) and otoacoustic emissions (OAE) were recorded in the guinea pig. An inner pressure increase of approximately 600 Pa gave only small changes in CMDP and DPOAE. Along with a decrease in f1 amplitude, a small decrease in amplitude of the 2f1 - f2 and a small increase in the f2 - f1 were measured in CM. This matches a shift from a symmetrical position of the operating point for hair cell transduction, leading to an increase in even-order distortion and a decrease in odd-order distortion. Similar, a decrease in 2f1 - f2 DPOAE was expected. This might be the case at the generation sites but this effect was then more than compensated for by a better middle ear transfer, accounting for the increase of 0.4 dB of the 2f1 - f2 DPOAE amplitude. In conclusion, changes of overall inner ear fluid pressure have minor effects on cochlear function. This is a relevant finding for further understanding of diseases with changed inner ear fluid volumes, as Ménière's.

Rupture of Reissner's membrane during acute endolymphatic hydrops in the guinea pig: a model for Ménière's disease?

CONCLUSION: The changes in cochlear function during a destructive acute endolymphatic hydrops were relatively small. This might be consistent with the hypothesis that an endolymphatic hydrops is a marker of disordered inner ear homeostasis rather than the cause of the clinical symptoms of Ménière's disease. OBJECTIVE: Assessment of cochlear function during induction of a destructive acute endolymphatic hydrops. MATERIALS AND METHODS: During repetitive microinjections of 0.5 microl of artificial endolymph at a rate of 50 nl/s the 2f1-f2 and f2-f1 cochlear microphonics distortion products (CMDP) and 2f1-f2 distortion products otoacoustic emissions (DPOAE) were recorded in the guinea pig. RESULTS: A 'catastrophe' occurred in the inner ear when 2.5-3.5 microl of artificial endolymph was injected. A rupture of Reissner's membrane was then found, most often in the apical turn of the cochlea. This rupture had only minor effects on the endocochlear potential, whereas it caused a marked decrease in 2f1-f2 DPOAE amplitude. The 2f1-f2 and f2-f1 CMDP amplitude increased during each injection prior to the rupture. After the rupture the f2-f1 CMDP amplitude decreased during each injection, possibly due to a shift of the cochlear transducer operating point position.

Changes in distortion of two-tone cochlear microphonic and otoacoustic emission signals during an acute endolymphatic hydrops in the guinea pig.

An acute endolymphatic hydrops was induced by the injection of 1.1 mul of artificial endolymph into the scala media of guinea pig cochleas. This volume corresponds with an acute endolymphatic hydrops of 23%. During and after the injection, cochlear function was assessed by measuring the 2f(1)-f(2 )and f(2)-f(1) distortion products in cochlear microphonics (CMDP) and the 2f(1)-f(2) distortion product otoacoustic emission (DPOAE). A reversible pressure increase of 23 Pa and a relatively stable endocochlear potential (EP) were accompanied by a mean decrease in 2f(1)-f(2) DPOAE of only 3.4 dB. Similarly, the 2f(1)-f(2) CMDP amplitude change was minimal during and after the injection. The only substantial change was measured in the f(2)-f(1) CMDP amplitude. The measured range of distortion amplitudes during an acute endolymphatic hydrops can be related to small changes in the cochlear transducer operating point.

Morphology of the endolymphatic sac in the guinea pig after an acute endolymphatic hydrops.

The role of the endolymphatic sac (ES) in endolymph volume homeostasis is speculative. The present study investigates changes of the ES's epithelia and luminal filling after induction of an acute endolymphatic hydrops. After microinjection of 1.1 mul artificial endolymph into scala media of the cochlea, guinea pigs were terminated immediately (n = 6) or after different time intervals ; 1/2 h (n = 3), 1 h (n = 4) and 2 h (n = 4). Inner ear specimens were processed for light and/or transmission electron microscopy. The non-injected contralateral ear served as a histological control. Correct injection was confirmed by detection of microspheres in the endolymphatic compartment after the same microinjection procedure. In all specimens, ribosome rich cells and intraluminal macrophages appeared to be actively involved in degradation of homogeneous substance (HS) by secreting lytic enzymes and digestion, respectively. Amazingly, in our study no ES differences were found between injected and non-injected ears and no distinct changes were observed in guinea pigs terminated after different time intervals. The ES's luminal HS was always present and often to a large extent. This is in contrast with [Hear. Res. 138, 81] dramatic changes were observed. Endolymph volume homeostasis is a complex mechanism, in which the role of HS remains obscure.

Effect of acute inner ear pressure changes on low-level distortion product otoacoustic emissions in the guinea pig.

OBJECTIVE: To determine a relation between acute inner ear pressure changes and cochlear function as measured by low-level 2f(1)-f(2) distortion product otoacoustic emissions (DPOAEs). MATERIAL AND METHODS: During and after a change in inner ear pressure induced by injection or aspiration of perilymph, the 2f(1)-f(2) DPOAE at 4.5 kHz generated by low-level primaries was recorded in the guinea pig. RESULTS: Large changes in overall inner ear pressure produced only small changes in the 2f(1)-f(2) amplitude and phase. During injection of 0.5 microl of artificial perilymph into the scala tympani over a 10-s period, the mean inner ear pressure increased by approximately 500 Pa, with an accompanying mean increase in the 2f(1)-f(2) amplitude of 0.7 dB. During aspiration of 0.5 microl of perilymph over a 10-s period, the mean inner ear pressure decreased by approximately 700 Pa, with an accompanying mean decrease in the 2f(1)-f(2) amplitude of 0.9 dB. Changes in DPOAE amplitude followed inner ear pressure changes with a delay of 1-2 s. The magnitude and sign of the amplitude changes can (partly) be explained by a change in oval window stiffness. No explanation was found for the measured delay. CONCLUSION: Clinically, these experiments can be of value in gaining insight into the pathophysiological mechanisms of pathological pressure changes as seen in Meniere's disease and perilymphatic fistulae.

The glycocalyx and stereociliary interconnections of the vestibular sensory epithelia of the guinea pig. A freeze-fracture, low-voltage cryo-SEM, SEM and TEM study.

In this study freeze fracture, low-voltage cryo-SEM, SEM and TEM were used to characterise the glycocalyx and stereociliary interconnections in the hair cell bundle of the vestibular sensory epithelia of the guinea pig. The glycocalyx resembles a shell-like structure separately surrounding each stereocilium and kinocilium over its entire length. The lateral interciliary connections emerge from the glycocalyx layer, forming an extensive extracellular network maintaining the stereocilia as a bundle. These connections are morphologically similar to the glycocalyx, and grossly oriented in the same direction, indicative of a role in the mechanical transduction system. The matrix material around the glycocalyx also appears to be morphologically similar to the glycocalyx, suggesting the glycocalyx to be even more important in the mechanical transduction system. The tip-links are covered with a layer, which is a continuation of the glycocalyx covering the stereocilia.

A second look at injection of vesical neck contractures with triamcinolone.

Adjuvant therapy for vesical neck contractures with triamcinolone injection has given good results with long-term followup but similar results have been obtained with transurethral resection alone in our current re-evaluation. Herein we review 220 consecutive vesical neck contractures treated by the aforementioned modalities.