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PubMed1984

Permeability to sodium ions of the endolymph-perilymph barrier.

The endocochlear potential and Na+ activity in the endolymph were simultaneously measured with a double-barreled Na+ selective liquid membrane electrode. The modified Na+ conductance and permeability coefficient of the endolymph-perilymph barrier were calculated from the rate of change in the endolymph Na+ concentration relative to the Na+ electrochemical gradient across the barrier during permanent anoxia. In normal guinea pigs the Na+ conductance of the endolymph-perilymph barrier is approximately 5 times less than its K+ conductance. Exposure to noise or treatment with kanamycin suppresses the cochlear microphonics but does not result in significant alterations in the Na+ permeability of the endolymph-perilymph barrier. It is likely that the Na+ permeability of the endolymph-perilymph barrier is not involved in the physiological processes which lead to the cochlear damage produced by noise or kanamycin.

Action Potentials↗
PubMed1993

Pharmacokinetics of furosemide in endolymph.

To investigate the pharmacokinetics of organic anions in the endolymph of the guinea pig, 100 mg/kg furosemide, an organic anion, was intravenously given to measure the concentration in the cochlear endolymph by high-performance liquid chromatography with fluorescence detection. In the endolymph, the concentration of the furosemide increased slowly for 1 hr to 1.6 micrograms/ml and gradually declined thereafter. Pretreatment with 200 mg/kg probenecid, an anion transport inhibitor, had no effect on the furosemide elimination in the endolymph except on the concentration at 2 hr. This was contrary to the drastic change observed in the perilymph of the scala tympani by the same pretreatment. Analogous to the effect in the endolymph, probenecid showed no change in the concentration of the serum, while a pronounced gradient of furosemide concentration existed between them. The present results suggest that the furosemide passively transfers from blood to the endolymph at a relatively low penetrability.

Animals↗
PubMed1997

Effects of high intensity impulse noise on ionic concentrations in cochlear endolymph of the guinea pig.

OBJECTIVE: To investigate the effect of acoustic overstimulation on concentrations of cations in cochlear endolymph and analyze the relationship between the ionic changes in endolymph and the hearing loss. METHODS: The endocochlear potentials (EP), K+, Na+ and Ca2+ concentration in cochlear endolymph were examined in vivo for normal and 167 +/- 2 dB SPL impulse noise exposed groups of guinea pig bored on time course by means of double-barreled ion-selective microelectrodes. Brain stem auditory evoked potential (BAEP) was used to evaluate the auditory function. Ca(2+)-ATPase activity was demonstrated cytochemically in the lateral cochlear wall as induced by Ando et al with slight modification. RESULTS: The K+ and Ca2+ concentration exhibited significant changes in 8-hour groups (P < 0.05 for K+ and P < 0.01 for Ca2+). Then the K+ concentration was eventually resumed to the initial levels in accordance with the EP recovery in 7 days, while during the same period Ca2+ concentration was always significantly higher than that in control group (P < 0.01). The BAEP threshold shifts were correlated well with changes in ionic concentrations, especially Ca2+ (P < 0.001), in the endolymph induced by acoustic trauma. Although the normal positive EP was observed 7 days after noise exposure, the function of the vascular stria was not completely restored as revealed by the fact that the Ca(2+)-ATPase was diffused to the apical membrane surface. CONCLUSIONS: Endolymph compartment intrinsic mechanism for maintaining ionic composition is seriously deteriorated after high impulse noise stimulation. The changes of the unique environment of endolymph may play an important role in the mechanism of sensorineural hearing loss induced by acoustic trauma.

Animals↗
PubMed1986

Direct measurement of longitudinal endolymph flow rate in the guinea pig cochlea.

The rate of longitudinal endolymph flow in the guinea pig cochlea has been measured with a novel tracer technique. The tracer we utilized was the tetramethylammonium (TMA) ion, the movement of which was monitored by ion-sensitive microelectrodes. Extremely small amounts of tracer were required as the electrodes could readily detect TMA concentrations in endolymph as low as 10 microM. TMA was introduced into scala media in the form of a small bolus, varying from 2-20 nl in volume. To examine whether longitudinal flow affects the dispersion of TMA in endolymph, we compared the characteristics of TMA spread to turn I following injection into turn II, with those of TMA spread to turn II following injection into turn I. The comparison of these data with an analytical model combining the processes of diffusion and volume flow demonstrates that the spread of tracer is dominated by passive diffusion processes with very little contribution from longitudinal endolymph flow. The rate of longitudinal endolymph flow between turn I and turn II was estimated to be less than 0.01 mm/min directed towards the basal turn. This value is considerably lower than recently published estimates using other techniques.

Cochlea↗
PubMed1982

K, Cl, and H2O entry in endolymph, perilymph, and cerebrospinal fluid of the rat.

The kinetics of radioactive potassium, chloride, and water entry into endolymph, perilymph, and cerebrospinal fluid were studied after intravenous administration of tracers in anesthetized and nephrectomized rats. Samples of cochlear endolymph, perilymph of scala vestibuli, perilymph of scala tympani, and cisternal cerebrospinal fluid were obtained. The data showed: 1) a rapid turnover of water in endolymph, perilymph, and cerebrospinal fluid, since 3H2O equilibrated with plasma in a few minutes; 2) a slow entry of 42K and 36Cl in perilymph, since 36Cl equilibrated with plasma after 2 h and 42K did not at 6 h; 3) an extremely slow entry of 42K and 36Cl in endolymph, since no equilibrium with plasma was obtained within the 5 h of the experiments. The comparison of the compartmental analysis of our data with the results of other studies using perilymphatic perfusion of tracers indicated that perilymph rather than plasma may be considered as the precursor of endolymph.

Animals↗
PubMed1989

Sodium transfer from endolymph through a luminal amiloride-sensitive channel.

An in vitro preparation of frog semicircular canal was devised to study the mechanisms of Na transport across the labyrinthine epithelium. When the lumen of the semicircular canal was filled with perilymph-like solution, the structure was able to secrete K into and to absorb Na from the lumen and to generate a lumen-positive transepithelial potential. When the lumen of the semicircular canal was filled with endolymph-like solution, the electrochemical composition of the luminal fluid was partly maintained up to 2 h. In this last experimental condition net and unidirectional fluxes were calculated in absence or presence of transport inhibitors, separately for the ampulla and for the nonampullar part of the canal. Amiloride (10(-5) M) but not dimethyl amiloride (10(-5) M) inhibited 60% of the unidirectional Na efflux out of endolymph; this Na efflux decrease resulted in an increase of the inward net Na flux. The net Na flux was also increased after abluminal application of ouabain (10(-3) M), furosemide (10(-4) M), and bumetanide (10(-6) M). This study validates this isolated preparation as a suitable tool for the study of endolymph secretion, confirms that the secretion of endolymph is achieved in the ampulla, and provides evidence for an apical amiloride-sensitive Na channel through which Na is transferred out of endolymph along an electrochemical gradient provided by the activity of the abluminal Na+-K+-ATPase.

Amiloride↗
PubMed1995

Comparison of endolymph cross-sectional area measured histologically with that measured in vivo with an ionic volume marker.

In order to establish how endolymph volume is regulated, it is essential to be able to measure endolymph volume or cross-sectional area in vivo. We have developed methods to accomplish this by injecting the volume marker ion hexafluoroarsenate (AsF6) into endolymph by iontophoresis. For an injection at a constant rate, the endolymph concentration is inversely dependent on the cross-sectional area of the scala into which injection occurred. Marker concentrations were monitored by inserting ion-selective microelectrodes into endolymph near the injection site. In a previous study we quantified the degree of hydrops in animals following ablation of the endolymphatic sac. In the present study we validated the technique by comparing the endolymphatic cross-sectional area measured in vivo with AsF6 with that measured by established histologic procedures. The correlation between the two measures was good, with a coefficient of .903, although the area measured histologically was a little lower than that measured in vivo.

Animals↗
PubMed1992

Characteristic ionic composition of endolymph is maintained in cultured inner ear.

Inner ear anlagen from mouse were explanted on the 16th gestational day (gd) and cultured for 5 days, i.e. corresponding to the time of birth. By using energy dispersive X-ray technique an elemental composition characteristic for endolymph was found within the membranous labyrinth of the explants. The sodium to potassium ratio in the endolymphatic space of the cultured inner ears corresponded to endolymph of the 16th gd fetus in vivo. There was no difference in the endolymph compartment between the cochlear and vestibular halves of the in vitro specimens. Differences in Na to K ratio between endolymph of the inner ears and the surrounding medium were statistically significant. Thus, endolymph-regulating mechanisms are active also under organ culture conditions, although not fully optimal.

Animals↗
PubMed1973

The mutual independence of the endolymphatic potential and the concentrations of sodium and potassium in endolymph.

The relationship between the endolymphatic potential (EP) and the sodium and potassium concentration gradients between endolymph and interstitial fluid was studied both by measuring the EP at varying concentrations of sodium and potassium in endolymph and by measuring the effect of a depressed EP on the concentrations of these cations. Ethacrynic acid was used in dogs to change the concentration of sodium and potassium (meq/liter) in endolymph from 5.8 and 148 to 134 and 24.3, respectively. No change in the EP accompanied these alterations. In a second series of experiments the EP was reduced from + 72 mV to + 31 mV for a mean duration of 20 min. No change in the concentration of sodium and potassium in endolymph was found during the period of reduced EP. These data suggest that there is little relationship between the EP and the sodium and potassium concentrations in endolymph.

Animals↗
PubMed1994

Transitory endolymph leakage induced hearing loss and tinnitus: depolarization, biphasic shortening and loss of electromotility of outer hair cells.

There are types of deafness and tinnitus in which ruptures or massive changes in the ionic permeability of the membranes lining the endolymphatic space [e.g., of the reticular lamina (RL)] are believed to allow potassium-rich endolymph to deluge the low [K+] perilymphatic fluid (e.g., in the small spaces of Nuel). This would result in a K+ intoxication of sensory and neural structures. Acute attacks of Ménière's disease have been suggested to be an important example for this event. The present study investigated the effects of transiently elevated [K+] due to the addition of artificial endolymph to the basolateral cell surface of outer hair cells (OHC) in replicating endolymph-induced K+ intoxication of the perilymph in the small spaces of Nuel. The influence of K+ intoxication of the basolateral OHC cell surface on the transduction was then examined. Intoxication resulted in an inhibition of the physiological repolarizing K+ efflux from hair cells. This induced unwanted depolarizations of the hair cells, interfering with mechanoelectrical transduction. A pathological longitudinal OHC shortening was also found, with subsequent compression of the organ of Corti possibly influencing the micromechanics of the mechanically active OHC. Both micromechanical and electrophysiological alterations are proposed to contribute to endolymph leakage induced attacks of deafness and possibly also to tinnitus. Moreover, repeated or long-lasting K+ intoxications of OHC resulted in a chronic and complete loss of OHC motility. This is suggested to be a pathophysiological basis in some patients with chronic hearing loss resulting from Ménière's syndrome.

Action Potentials↗
PubMedDate not supplied

Calcium gradients in inner ear endolymph.

Recent studies suggest that endolymphatic hydrops resulting from the ablation of the endolymphatic duct and sac in guinea pigs may be caused by a disturbance of endolymph calcium homeostasis. A similar disturbance of calcium homeostasis could represent the underlying cause of Ménière's disease. In this study, we mapped the calcium concentrations and electrical potentials throughout the endolymphatic system in normal guinea pigs. Large concentration differences exist between different compartments, including a more than twofold increase along the length of the cochlea. The electrochemical potential for calcium (the force driving passive longitudinal calcium movement) was calculated for all the endolymphatic compartments. The results show that endolymph is extremely inhomogenous with respect to calcium potentials. On the basis of these potentials, it appears that calcium is transported into endolymph in the cochlea and out of endolymph in the saccule and utricle. The possibility that endolymphatic hydrops arises from a disturbance in longitudinal flow of calcium, rather than in longitudinal volume flow, is considered.

Animals↗
PubMed1987

The Ca2+ activity of cochlear endolymph of the guinea pig and the effect of inhibitors.

The Ca2+ concentrations in cochlear perilymph and endolymph of the guinea pig were measured with double-barreled Ca2+-selective microelectrodes and showed 1.76 +/- 0.74 X 10(-3) M and 2.20 +/- 0.19 X 10(-5) M, respectively. The electrochemical potential gradient for Ca2+ between perilymph and endolymph was 23.2 mV and the existence of an active transport mechanism from the former to the latter was suggested. Vanadate given perilymphatically decreased the Ca2+ concentration in endolymph with a slight elevation of the endocochlear potential and was suspected of blocking the active transport. The Ca2+ concentration in endolymph was abruptly increased by anoxia or the intravenous administration of 60 mg/kg furosemide and was slightly increased by the intravenous administration of 30 mg/kg furosemide or 100 mg/kg acetazolamide. The endolymphatic pH measured with pH-microelectrodes under various conditions indicates that the mechanism of increase in the Ca2+ concentration is attributed not to the liberation of Ca2+ from the surrounding tissues caused by a fall in pH but to the increased influx of Ca2+ from perilymph due to the depression of the endocochlear potential.

Acetazolamide↗
PubMed1987

Longitudinal flow of endolymph measured by distribution of tetraethylammonium and choline in scala media.

Longitudinal endolymph flow rate in the guinea pig cochlea was measured by determining the rate of migration of extrinsic ions, tetraethylammonium chloride (TEA) or choline, with a potassium sensitive ion-selective microelectrode (ISM). Low concentrations of iontophoretically injected TEA were detected with the ISM at various distances from the injection electrode. The results were variable when the ISM was used to record spread of TEA from turn II to turn I and vice versa. However, consistent data were obtained when the TEA spread was measured at different electrode separations (0.2, 0.5, 0.7 mm) within turn II. Electrode locations were systematically exchanged without changing their distance, i.e. the ISM electrode was placed basally or apically with respect to the TEA electrode. Comparison of data with a model, which combines the bulk diffusion of TEA and the flow of endolymph, is consistent with a rate of endolymph flow in turn II of about 0.2 mm/min, apex to base. A similar value was also obtained with the iontophoretic injection of choline. The endolymph flow rate may be different in turn I as indicated by measurements of compound action potential (CAP) changes. However, the results of experiments when TEA spread is measured at large distances must be interpreted cautiously because TEA may enter cellular walls of the cochlear duct and alternative routes of transport may be involved.

Action Potentials↗
PubMed1987

Early effects of acetazolamide on anionic activities of the guinea pig endolymph: evidence for active function of carbonic anhydrase in the cochlea.

The effect of acetazolamide (ACZ) on HCO3- and Cl- activities in inner ear fluid was investigated by ion-selective microelectrode methods. The endocochlear potential, at 81.6 +/- 1.5 mV under normal conditions, was reduced by 4.9 +/- 0.9 mV in 30 min following the ACZ injection. The HCO3- concentrations by 11.5 +/- 1.7 mM in 30 min, while the change of Cl- level was not consistent but showed a tendency toward slight increase in average. The calculated PCO2 in endolymph was 39.6 mmHg. ACZ induced a constant elevation of the endolymph PCO2, with an increase in the venous PCO2 during the initial 20 min and thereafter the endolymph PCO2 attained a plateau despite the continuous increase of the venous PCO2. We postulate that the HCO3- secretion into the endolymph is mediated by carbonic anhydrase (CAH) and is decreased by ACZ due to the inhibition of CAH.

Acetazolamide↗
PubMed1994

Time course of endolymph volume increase in experimental hydrops measured in vivo with an ionic volume marker.

A new method has been developed to measure the cross-sectional area (CSA) of scala media in the living cochlea. The method has some advantages over histological methods, in which tissues may shrink or move during processing. In the present study, scala media CSA was measured in the second turn of guinea-pig cochleas in which endolymphatic hydrops was induced surgically. The area measurement method used an iontophoretic injection of a volume marker into scala media, during which the concentration of marker in endolymph was monitored with an ion-selective microelectrode. The measured marker concentration was inversely proportional to the CSA of endolymph. The marker we used was the anion arsenic hexafluoride (AsF6-), which was almost ideal for the purpose as it was retained well in endolymph. Area was measured in normal animals and in hydropic animals at times from 4 days to 16 weeks after endolymphatic duct obstruction. The results showed that hydrops develops within days of ablation of the endolymphatic duct. The degree of hydrops was compared with electrophysiological measures of function, including the endocochlear potential, action potential thresholds and the amplitudes of the cochlear microphonic, summating potential and action potentials. In the initial stages of hydrops development, electrophysiological changes were small. In contrast, there were marked functional changes between 8 and 16 weeks, when endolymph volume was no longer increasing. If the same is true for dysfunction in the ears of patients with Ménière's Disease, then it may not be possible to restore normal function simply by alleviating the hydrops.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed2006

Characterization and variations of organic parameters in teleost fish endolymph during day-night cycle, starvation and stress conditions.

The aim of the present work was to examine the modifications of the organic composition of fish endolymph under environmental conditions (day-night cycle, starvation and Cl2-stress) known to modify otolith growth. Endolymph electrophoretic patterns were compared. An antibody raised against the trout otolith organic matrix allowed examining the variations of organic matrix precursors in the endolymph under the above conditions. Western blot analysis showed bands around 60-80 kDa. A 50% decrease of immunolabelling was observed during the night whereas increases were seen after starvation (factor 3) or stress (factor 2) suggesting that these variations could be related to the organic matrix deposit. A factor retarding in vitro CaCO3 crystallization (FRC) was shown to co-precipitate with endolymph proteins and its apparent molecular mass (determined by measuring the activity after electro elution of gel electrophoresis) was estimated around 20 kDa. The FRC activity was stable during day-night cycle whereas it decreased by 70% and nearly 100% under starvation and stress respectively. These results suggest that the FRC, although retarding in vitro crystallization, plays a major role in the process of otolith calcification and that the decreases measured after starvation and stress are responsible for the decreases of the otolith growth. The variations of these two parameters (precursors and FRC) could contribute for the changes in the microstructure of the otolith.

Animals↗
PubMed1998

Effect of artificial endolymph injection into the cochlear duct on the endocochlear potential.

We investigated the effect of acute endolymphatic hydrops on the positive endocochlear potential (+EP) and negative endocochlear potential (-EP). The +EP was measured in guinea pigs during injection (without outlet) and perfusion (with outlet) of artificial endolymph into the cochlear duct. The -EP was measured during anoxia after the injection or the perfusion had finished. Injection of artificial endolymph produced a slight transient increase in the +EP, and a significant decrease in the magnitude of the -EP. Chronic endolymphatic hydrops produces both +EP and -EP decrease. The +EP decrease in chronic endolymphatic hydrops may cause the chronic change of the inner ear. The +EP increase in acute endolymphatic hydrops may be caused by a shift of the basilar membrane. However, the mechanism of the 'transient' +EP increase is not clear. The -EP decrease was not observed in animals whose cochlear duct was perfused with artificial endolymph. Therefore, the artificial endolymph itself did not cause the decrease in magnitude of the -EP. Dysfunction of the hair cells is a possible explanation for the -EP decrease but the mechanism of such a decrease is not clear in the present study. However, the results of this study support the notion that small increases in endolymphatic pressure below the resolution of recent measurements (DeMott and Salt, 1997) can lead directly to a reduction of the -EP during hydrops. The animal model described here can eliminate the chronic effect of hydrops, therefore, this model is useful for investigations into the effect of hydrops itself on the inner ear and the mechanism of hearing loss in Ménière's disease.

Action Potentials↗
PubMed1999

Morphological changes of the endolymphatic sac induced by microinjection of artificial endolymph into the cochlea.

Morphological changes of the endolymphatic sac were analyzed in guinea pigs following microinjection of artificial endolymph into the cochlea or withdrawal of a quantity of native endolymph. Injections were performed into the second turn of scala media with a micro-pump at a rate of 60-100 nl/min, lasting for a period of 4, 7. 5, 15 or 18 min. In withdrawal experiments, endolymph was aspirated from the second cochlear turn over a period of 8 min. For each procedure the contralateral (non-treated) ear served as a histological control. Following artificial endolymph injections of 7. 5 min or more there was an almost total absence of the normal intraluminal homogeneous substance (HS) on the injected side. Our observations suggest that the disappearance of the HS occurs by both enzymatic and macrophagic activity. After endolymphatic withdrawals the ES was found to contain increased amounts of HS. The results could suggest that the volume of fluid in the ES, and hence the volume of the entire membranous labyrinth, may be regulated by a dynamic relationship between active secretion and enzymatic degradation of a lumen-expanding substance that is intimately related to the intraluminal macrophages. The exact mechanism governing these regulatory systems, and their relationship to ion and water movements across the epithelium of the sac, remain to be elucidated.

Animals↗