Acta Oto-Laryngologica

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Damage To The Stria Vascularis In The Guinea Pig By Acute Atoxyl Intoxication M. Anniko & J. Wersäll To cite this article: M. Anniko & J. Wersäll (1975) Damage To The Stria Vascularis In The Guinea Pig By Acute Atoxyl Intoxication, Acta Oto-Laryngologica, 80:1-6, 167-179, DOI: 10.3109/00016487509121316 To link to this article: http://dx.doi.org/10.3109/00016487509121316

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Acta Otolaryngol80: 167-179, 1975

DAMAGE TO THE STRIA VASCULARIS I TI E GU BY ACUTE ATOXYL INTOXICATION

IEA PIG

M. Anniko and J. Wersall From the Department of Otolaryngology, Huddinge Sjukhus, and King Gustav V Research Institute, Stockholm, Sweden

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(Received April 1, 1975)

Abstract. The aim of the present study was to show the morphological degeneration at the ultrastructural level, after damaging the stria vascularis experimentally. The acute lesions, after acute atoxyl intoxication, occur after about 12 hours, and begin as a degeneration of both the marginal and the intermediate cells, whereas the basal cells remain mainly unaffected. The severely damaged marginal or intermediate cells may become loosened from the stria vascularis and rejected from it into the endolymphatic space. Under such conditions the basal cells may line the surface facing the endolymph, although this occurs very rarely. Initially, there may be a slight bulging of Reissner’s membrane, but soon the membrane becomes depressed, and sometimes a total collapse occurs, with Reissner’s membrane flattened over the tectonal membrane against the organ of Corti. It is only seldom that Reissner’s membrane touches the strial surface. Mitochondria1 degeneration with formation of intramitochondrial inclusion bodies is a n interesting early finding in the damage pattern.

In 1851 Alphonse Corti described the stria vascularis as a capillary network closely surrounded by epithelial cells. Nowadays, it is well known that three different types of epithelial cells are found in the stria, the dark (chromophil or marginal), the light (chromophobe or intermediate) cells, and the basal cells (v. Fieandt & Saxen, 1937; Engstrom et al., 1955; Smith, 1957; Bairati & Iurato, 1960). On the basis of the ultrastructural features it may be assumed that the stria, an extremely highly differentiated tissue, is able to This work was supported by grants from the Karolinska lnstitutet and from the Swedish Medical Research Council (grant no. 12X-720). I2 -752953

perform a selective secretory activity and to a lesser extent, some resorptive function (Spoendlin, 1967). In 1938 Hallpike &L Cairns were the first to describe the histological picture in Meniere’s disease. They found gross dilatation of the scala media and degneneration of both Corti’s organ and the stria vascularis. Recently the functional pathology of the stria vascularis has aroused renewed attention following the demonstration of strial damage in experimental animals treated with ethacrynic acid by Quick & Duvall (1970). Nakai (1971) also reported strial changes due to ethacrynic acid. The toxic effect of the arsenic compound, atoxyl, on inner ear structures was described by Miayamoto (1931). H e found histopathologic abnormalities in the organ of Corti and the stria vascularis. Nakamura (1935), Ozeni (1937) and Riiedi (1951) confirmed these findings. The effects of arsacetin (acetylated atoxyl) were first studied by Causse et al. (1940), who recorded loss of the Preyer’s reflex and the cochlear microphonics, and delayed vestibular disturbance. Similar findings were obtained by Leonard et al. (1971). Johansen (1953) reported marked histopathologic changes after arsacetin administration, involving the organ of Corti and the stria vascularis. The purpose of the present study was to Acta Otolatyngol80

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M . Anniko and J . Wersall

Table I. Diagram illustrating the doses injected into the guinea pigs of the experimental group

No.

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20 52 53 54 55 63

Mg/kg at each injection 70 70

I00 70 140 140

Number of injections

Injected during (days)

3 2 1 2 1 1

2 1 4

Totally mg/k

Killed after the last injection (days)

210 140

i

100 1 4

140 140 140

investigate the toxic effects of atoxyl on the stria vascularis with special regards to the question whether atoxyl is a suitable substance for experimental studies of stria1 function and pathology.

MATERIALS AND METHODS Nine young, healthy guinea pigs, with normal Preyer’s reflex, weighing aroung 250-350 grams, were used for the experiment. Six animals were injected with atoxyl. The control group consisted of 3 healthy, non-injected guinea pigs.

Administration of atoxyl Each animal was given a 2 % solution of atoxyl in sterile water subcutaneously during a certain period of time. The dosage varied between 70 and 140 mg atoxyl per kg body weight. The total dose ranged from 100 to 210 mg per kg body weight. The duration of administration varied between 6 hours and 2 days and the survival time before decapitation between 6 hours and 1 day after the last injection (Table I). Morphological procedures For microscopy, specimens were taken according to the technique of Wersall(l956) with Acta Otolaryngol80

1

Preyer reflex

-

t

(+I (+I

B

-

1 1

-

decapitation of the animal. The temporal bones were removed, and an opening was made in the bulla tympanica. The stapes was extracted, the round window membrane opened, and a small opening made at the apex to allow sufficient penetration for fixation. The cochlea was perfused with 2% buffered osmium tetroxide solution through the opening in the apical coil of the cochlea. The specimen was immersed for 2 hours in the fixation fluid, then dehydrated in alcohol, and embedded in epon. 1 pm thick sections, stained with toluidene blue, were studied in the light microscope. Thin sections were analysed in the electron microscope after staining with uranyl acetate and lead acetate.

RESULTS Structural alterations may be observed in some parts of the stria vascularis even approximately 12 hours after the administration of atoxyl. After 24 hours, severe degeneration occurs in all the turns of the cochlea (Fig. 1). After treatment with 70 mg atoxyl per kg body weight, and repeating the same dose after 6 hours the animal was killed 12 hours after the first injection. The apical turns were severely affected whereas the basal coil showed only minimal changes. The same changes were

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Damage to stria vascularis by atoxyl intoxication

Fig. I. (a-d) Different stages of strial degeneration. Light microscopy. Magnification 2 8 0 ~The . stria vascularis initially become swollen (a, 3rd coil, animal No. 20) and later marginal and intermediate cells are rejected from the

strial surface (b, c, 3rd coil, animal No. 52). The position of Reissner’s membrane is altered and it becomes depressed and lies over the organ of Corti in the final stage (d, 3rd coil, animal No. 54). , Acta Otolavngol80

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Fig. 2. Heavily degenerating intermediate ( I ) cells in the stria vascularis. The blood vessel ( B ) is blocked by red blood cells (3rd coil, animal No. 20). EMG. Acru Otolaryngol 80

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Damage to stria vascularis by atoxyl intoxication

observed when 140 mg atoxyl per kg body weight were administered, and the investigation was made 24 hours after the injection. Observations after only 12 hours showed an almost normal morphological structure. An injection of 100 mg atoxyl per kg body weight, and the specimen studied after 24 hours, caused only minimal degeneration in the stria vascularis, except in the apical coil. Severe degeneration of the stria vascularis occurred when 70 mg atoxyl per kg body weight was administered three times within 36 hours, and the guinea pig killed 48 hours after the first injection. In these specimens the stria of all the coils was so severely damaged that no coil was observed to predominate. The damage areas may be localized or diffused. Lesions occurred near both the blood vessels in the stria vascularis, and the spiral prominence, the latter being the most frequent site. Among the three types of stria1 cells, the marginal and intermediate cells were most frequently affected (Fig. 2). The degeneration of marginal and intermediate cells followed the same pattern. Different degrees of vacuolization appears early (Figs. 2 and 3 b) which may become so extensive that almost the whole cell is filled up by vacuoles, and the degenerating cell organelles and nucleus are pressed towards the peripheral parts of the cell body. The normal cell appearance, with cytoplasm densely packed with mitochondria, especially in the basal part, and Golgi membranes, was lost at an early stage during degeneration. The normally irregular, chromatin-rich nucleus was the last component to disintegrate by swelling, chromatin fragmentation and, finally, by rupture of the nuclear membrane. The mitochondria undergo swelling, and accumulation of dense material occurred between the cristae (Fig. 3 a). One or more such accumulations can be found in almost every damaged mitochondrion, but they occupy only a minor portion of it. These changes occur relatively soon in the initial phase of mitochondrial degeneration. Thus, the cristae mitochondriales are still

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often preserved, although they are irregular and fragmented. In some cases the dense material occupied a major part of the mitochondrial volume. In a few cases mitochondrial degeneration, with formation of lamellated bodies, occurred. While these degenerative processes were taking place there was a tendency for the rejection of the severely damaged cells from the stria vascularis into the endolymph (Fig. 4 a, b). Not all the marginal cells, however, that become damaged undergo all the phases of degeneration before they are loosened from the stria. A cell may be rejected also at an earlier stage, whereas some cell organelles and fragments of the nucleus may still be recognized. The lining facing the endolymph will, therefore, consist of both marginal and intermediate cells and, to a lesser degree, also of basal cells. The loosening of the marginal cells from the stria vascularis is more manifest towards the spiral prominence, but is also observed around the vessels in the stria to a great extent. The area around the insertion of Reissner’s membrane is not so severely affected. Some of the rejected cells are so severely damaged that it is impossible to recognize their origin (Fig. 5). There are findings which indicate that the intermediate cells may be affected first. In several serial sections starting at the stria vascularis and proceeding towards the spiral ganglion, rather severely degenerating intermediate cells may be observed, whereas the processes of the marginal cells appear lo be only slightly damaged. In the cell cytoplasm of many intermediate cells there are accumulations of colloid-like, dense material (Fig. 3 b) of the size of several mitochondria. Nothing of the ordinary endoplasmatic reticulum or ribosomes can be observed. Severely damaged intermediate cells are rejected from the stria vascularis in the same way as in the marginal cells. The melanin pigment participates ip the rejection process either as a component of the rejected cell, or it may also be found in the endolymph Acta Otolaryngol80

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Fig. 3. (a) Intermediate cell with vesiculation and degenerating mitochondria ( M ) containing electron-dense material (3rd coil, animal No. 20). EMG. (b) Intermediate Actu Otolaryngol80

( I ) cell with lipoid-like material ( L ) in the cytoplasm, vesiculation and mitochondria1 degeneration (3rd coil, animal NO. 20). EMG.

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4 Fig. 4 . (a) Advanced stage of the rejection of heavily degenerating marginal and intermediate cells (2nd coil, animal No. 52) EMG. (b) Early stage of the rejection of a

moderately damaged marginal ( M ) cell. The blood vessels ( B ) are blocked by red blood cells. The basal cells (BC) appear normal (2nd coil, animal No. 54). EMG. Acta Otolaryngol80

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Fig. 5. Loosening of heavily degenerating marginal and intermediate cells from the surface of the stria vascularis. Acta Otolaryngol80

The basal cells (BC) remain unaffected (3rd coil, animal No. 52). EMG.

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alone, probably as the result of a completely cernible. Among the strial cells the earliest and most frequently affected are both the mardisintegrated cell. The flat, tightly packed basal cells, with ginal and the intermediate cells and it has so their sometimes gigantic intracellular vacu- far not been possible to assert with certainty oles, are very little affected by acute atoxyl which cell type degenerates first. However, in intoxication. However, not until the marginal some specimens the intermediate cells are and the intermediate cells have degenerated more severely affected than the marginal cells. and become loosened from the stria vasBoth marginal and intermediate cells may cularis, and the adjacent marginal and in- become loosened from the stria vascularis and termediate cells are unable to stretch and fill float out into the endolymph. At the same up the missing cell spaces, do the basal cells time, pigment is also liberated, so that it flows become involved in the lining towards the en- out into the endolymph. Here and there, cells dolymphatic space. may be seen to burst and discharge their conThe strial vessels are often blocked by tent of pigment. The degeneration of the stria dense accumulations of blood cells. In a few vascularis may occur in all parts of the true blood capillaries, small lamellated bodies may stria vascularis, although there is a predilecbe observed near the nucleus in the endothelial tion for the zone near the spiral prominence, cell. In acute atoxyl intoxication an intercellu- and that near the blood vessels. The reason for lar space around the blood vessels in the stria the vulnerability of these areas is not clear but vascularis is a rather constant finding (Fig. 6). it is likely that there may be a high concentraNo such space is found in the control group. tion of the substance around the vessels. Mygind & Dederling (1932) and Hallpike & During the early stages of atoxyl administration, Reissner’s membrane initially becomes Cairns (1938) were the first to describe the slightly bulging, but this stage is soon followed distention of the cochlear duct in histological by depression of the membrane, so that it be- specimens, as evidenced by the bulging of discomes flattened over the tectorial membrane placed Reissner’s membrane. These findings against the organ of Corti. When Reissner’s have been confirmed by Hallpike & Wright membrane is collapsed it covers the tectorial (1940), Rollin (1940), Lindsay (1942) and Altmembrane and the Hensen cells, but it very man & Fowler (1943), so that the term ‘enseldom touches the stria vascularis itself (Fig. dolymphatic hydrops’ is generally accepted as 1). Although all the coils of the cochlea are a synonym for Meniere’s disease. In the acute affected, the findings are more pronounced at atoxyl-intoxicated guinea pig there is a the apical coils. Between this extreme position tendency for a slight hydrops to occur initially, of Reissner’s membrane, as described above, but the slightly bulging Reissner’s membrane and its normal position, all kinds of in- is very soon depressed, and subsequently, it termediate stages may be found. collapses to a considerable extent. Altman (1961) stated that the dilatation of the endolymphatic system appears to be the result of an increased endolymphatic pressure, probaDISCUSSION bly due to a change in the chemical constituThe present investigation shows that the stria tion of the endolymph by an accumulation of vascularis in atoxyl-treated guinea pigs under- molecules causing a light osmotic pressure in goes different stages of degeneration of the the endolymph. In acute atoxyl intoxication marginal and the intermediate cells. The stria the initial phase with hydrops is extremely may initially appear normal under the light short in relation to the phase of strial cell demicroscope, but under the electron micro- generation. scope morphological alternations are disQuick & Duvall (1970) reported changes in Acta Otolunwgol80

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176 M . Anniko and J . Wersall

Fig. 6 . Stria1 blood vessel with surrounding intercellular space ( I ) (2nd coil, animal No. 20). EMG.

the sttia vascularis after high doses of ethacrynic acid whereas smaller doses did not produce any anomalies. There was an increase in the thickness of the stria vascularis due to intracellular and extracellular edema. The marginal and the basal cells looked normal. The intermediate cells were either completely destroyed, or in an advanced stage of atrophy. The melanin granules, normally contained within the intermediate cells, seemed resistant to atrophy. Nakai (1971) reported, however, that ethacrynic acid intoxication mainly affected the marginal cells of the stria vascularis. Contrary to the damage to the sensory cells in the organ of Corti, the changes in the stria vascularis had disappeared in cases that were observed for long ,periods after final administration. Whereas the ethacrynic acid degeneration of the stria1 cells apparently is reversible Actu Otoluryngol80

in the early stage of toxic reaction the changes found after atoxyl intoxication are mainly of irreversible type. Kimura & Schuknecht (1970) found in patients with Meniere’s disease that the earliest and most frequent changes were in the marginal cells by decrease in cytoplasmic density, reduction in the number of mitochondria, pinocytotic vesicles, and rough endoplasmatic reticula. The intermediate cells were less frequently effected but similar changes occurred. As tha marginal cell layer thinned out, the intermediate cells grew and occupied the major portion of the stria. The basal cells were least affected. When the marginal and intermediate cells disappeared, the basal cells often remained intact, thus the endolymphatic surface emerged. The general finding was that, as the thickness of the stria vascularis decreases, the extent of the pathology increases.

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Damage to stria vascularis by atoxyl intoxication

Similar findings, concerning the basal cells, were made in connection with atoxyl treatment. Hilding (Kichuchi & Hilding, 1965; Hilding et al. 1967) reported that the mitochondria, ribosomes, Golgi complexes and endoplasmic reticula are seen, within normal range, in the stria vascularis up to 4 weeks of age in the Shaker-1 mouse. However, these structures then started to become less numerous, and degenerative changes appeared. Leonard et al. (1971) studied the effects of damage to the organ of Corti and the stria vascularis, on endolymphatic cationic changes due to treatment with arsacetin. Arsacetin was chosen in view of its established ability to damage both the stria vascularis and the organ of Corti by altering the components of the scala media. Depression of cochlear microphonics (CM) was found in many animals. The histopathological appearance of the organ of Corti was abnormal in all instances in which the Preyer’s reflex or CM were altered. In animals with depression of the endolymphatic, direct-current potential (EP), light-microscopic investigation showed that the stria vascularis appeared to have been damaged. In the total histopathological study, no iiolated instances of damage to the stria vascularis alone could be observed. Tasaki & Spyropoulous (1959) assumed that cochlear microphonics (CM) originate from the hair cells of the organ of Corti, and that the endolymphatic, direct-current potential (EP) originates from the stria vascularis. Investigations by Matschinsky & Thalmann (1967) and finally by Kuijpers (1969) have clearly shown that the marginal cells are involved in the removal of sodium from the endolymph and are also emitting potassium into this fluid, thereby restoring and maintaining the important electrolyte composition of the endolymph. Disturbance of the metabolism of the marginal cells, which are assumed to be engaged in fluid transport (Spoendlin, 1967), must interfere with endolymph production and, to a lesser degree, also with reabsorption. The subsequent degeneration of the margi-

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nal cells, resulting in their rejection, will thus block the endolymph circulation, and the electrolyte balance will collapse. This must interfere with the position of Reissner’s membrane, which becomes depressed. A simple rupture at some point cannot result in the general depression of the whole membrane in all its coils. It is apparent that a passage of fluid through Reissner’s membrane is not sufficient to allow for a normal location of this membrane. Lawrence (1964) established that perforation of Reissner’s membrane at single points causes no damage to the stria vascularis, but the perilymph is absorbed at the local level around the perforation. However, damage was noted in the cells, on the basilar membrane, nearest to the perforation. As expected, primary lesions of the stria, caused by a substance reaching the stria, might be supposed to appear via the bloodstream equally distributed in all turns of the cochlea. However, in several guinea pigs the severest changes were found in the apical coils, whereas the basal turn, although damaged, was not so severely affected. Similar findings were described by Kimura & Perlman (1958) and by Bernstein & Silverstein (1966) by the obstruction of labyrinthine vessels. Kimura & Perlman (1958) found that after arterial obstruction the stria vascularis appeared to become partly detached from the spiral ligament as one unit, without edema, hemorrhage or dilation of the vessels. After venous obstruction the stria did not become partly detached, but edema, vascular dilation, and fragmentation occurred. The stria vascularis finally disappeared, and was replaced by low, flat epithelium. The stria in the region adjacent to the round window changed more slowly. The position of Reissner’s membrane remained unchanged throughout. However, Bernstein & Silverstein (1966) found a collapse of Reissner’s membrane, especially in the apical turns. Stria1 atrophy of the ageing ear is well documented by Schuknecht (1955) and by Schuknecht & Igarashi (1964). It is charActa Otolaryngol80

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178 M . Anniko and J . Wersall

acterized by degenerative changes, however, which begin at the basal end of the cochlear duct and proceed towards the apex, affecting almost equally and simultaneously the various structures within the duct. The finding of an intercellular space sometimes around the blood vessels in the stria vascularis, in connection with atoxyl treatment, is rather obscure. Spoendlin (1967) summarized the general opinion concerning the stria vascularis, and stated that such findings are usually regarded as due to fixation artefacts. There was no such space, however, surrounding the blood vessels in the control material, although it was treated in the same way in the fixation fluid. The term intercellular space is, to some extent, misleading, because arsenicals in general cause damage to blood vessels (Osol & Pratt, 1973). Consequently, the blood vessel is surrounded by blood colloids and electrolytes, hereby causing separation of the marginal-cell extentions from the capillary wall. The intercellular space would, therefore, be the result of increased capillary permeability. The changes found in the stria vascularis indicate that the stria vascularis is one primary site of action of atoxyl. A degeneration of the stria4independent of reason for the degeneration is invariably followed by hair cell damage. The objective of further studies on the material will be to correlate stria1 damage with cochlear hair cell degeneration in various parts of the cochlea and its physiological significance. ACKNOWLEDGEMENT The authors wish to express their appreciation to Mrs Mane-Louise Spangberg for skilful technical assistance.

ZUSAMMENFASSUNG Die Absicht der vorliegenden Untersuchung ist es, auf ultrastrukturellem Niveau die morphologische Degeneration der Stria vascularis nach experimenteller Schadigung darzustellen. Die akute Schadigung nach akuter Atoxylintoxikation tntt nach ca. 12 Stunden auf und beginnt als Degeneration der marginalen und intermediaren Zellen, Acta Otolaryngol80

wahrend die basalen Zellen im wesentlichen intakt bleiben. Die stark geschadigten marginalen oder intermediaren Zellen kiinnen von der Stria vascularis abgelost und in den endolymphatischen Raum abgestossen werden. In solchen Fdlen bekleiden die basalen Zellen die Oberflache zur Endolymphe, wenngleich dies auch sehr selten vorkommt. Nach anfanglicher leichter Vorwolbung der Reissnerschen Membran kommt es bald zu einer Senkung und in manchen Faillen zu einem volligen Kollaps der Membran, wobei die Reissnersche Membran uber der Membrana tectoria gegen das Cortische Organ hinabgeflacht ist. Nur in seltenen Fdlen beruhrt die Reissnersche Membran die striale Oberflache. Eine Degeneration der Mitochondnen mit Bildung von intramitochondrialen EinschluBkorperchen ist ein interessanter Friihbefund des Schadigungsmusters.

REFERENCES Altman, F. 1961. Menikre’s disease. JAMA 176, 215. Altman, F. & Fowler, E. P., jr 1943. Histological findings in Meniere’s symptom complex. Ann Otol Rhinol Laryngol52, 52. Bairati, A., jr & Iurato, S. 1960. Sulla struttura submicroscopica delle zone dell ’epitelio del labirinto membranoso addette alla produzione dell ’endolinfa. Monitore Zoo1 Ztal, Suppl. 68, 245. Bernstein, J. M. & Silverstein, H. 1966. Anterior cerebellar and labyrinthine arteries. A study in the cat. Arch Otolaryngol83, 422. Causse, R. et al. 1949. Modification des potentiels cocleaires du Cobaye sous l’influence de l’acide acetylaminophenylarsinique (arsacetine). C R Soc Biol (Paris) 143, 68. Corti, A. 1851. Recherches sur l’organe de l’ouie des mammieres, 2 Wiss Zool, 3 , 109. Engstrom, H., Sjostrand, F. S. & Spoendlin, H. 1955. Feinstruktur der Stria Vascularis beim Meerschweinchen. Pract Otorhinolaryngol (Basel) 17, 69. Fieandt, H. von & Saxen, A. 1937. Beitrage zur Histologie der Stria vascularis und der Prominentia spiralis bei Saugern (Hund und Mensch). Z Anat Entwicklungsgesch 106, 424. Hallpike, C. S. & Cairns, H. 1938. Observations on the pathology of Meniere’s syndrome. J Laryngol Otol53, 625. Hallpike, C. S. &Wright, A. J. 1940. On the histological changes in the temporal bones of a case of Meniere’s disease. J Laryngol Otol55, 59. Hilding, D. A., Sugiura, A. & Nakai, Y. 1967. Deafwhite mink: electron microscopic study of the inner ear. Ann Otol Rhinol Laryngol76, 647. Johansen, H. 1953. Studies on the effect of arsacetin on the labyrinth. In Proc Fifth Int Congr Otolaryngol, pp. 579-585. Kikuchi, K. & Hilding, D. A. 1965. The defective organ of Corti in Shaker 1 mice. Acta Otolaryngol (Stockh) 60, 287. Kimura, R. & Perlman, H. B. 1958. Arterial obstruction of

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Damage to stria vascularis by atoxyl intoxication the labyrinth. Part I. Cochlear changes. Ann Otol Rhinol Laryngol67, 1 . Kimura, R . S. & Schuknecht, H. F. 1970. The ultrastructure of the human stria vascularis, Part 11. Acta Otolaryngol (Stockh) 70, 301. Kuijpers, W. 1969. Cation transport and cochlear function. Thesis, Centrale Drukkerij, Nijmegen. Lawrence, M. 1964. Endolymph-perilymph diffusion after barrier breakdown. Arch Otolaryngol 79, 366. Leonard, J . E., Nakashima, T . & Snow, J . B. 1971. The effects of damage to the organ of Corti and the stria vascularis o n endolymphatic cationic changes. Arch Otolaryngol94, 54 1 . Lindsay, J. R. 1942. Labyrinthine dropsy and Meniere’s disease. Arch Otolaryngol35, 853. Matschinsky, F. M. & Thalmann, R . 1967. Quantitative histochemistry of microscopic structures of the cochlea. Ann Otol Rhinol Laryngol76, 638. Miayamoto, T . 1931. Experimentelle Untersuchungen iiber die Schadigung des Gehororgans durch die Giftwirkung der Arzneimittel: Die Wirkung des Atoxyls auf das Gehororgan, Arbeiten aus der Medizinischen Universitut Okayama, 2 (3). Okayama, Japan. Mygind, S. H. & Dederling, D. 1932. The significance of water metabolism in general pathology as demonstrated by experiments on the ear. Acta Otolaryngol 17, 424. Nakai, Y. 1971. Electron microscopic study of the inner ear after ethacrynic acid intoxication. Pract Otorhinolaryngol (Basel) 33, 366. Nakamura, H. 1935. Experimentelle Untersuchungen iiber die Fettsubstanzen in Gehororgan: 11. Mitteilung: iiber die Fettsubstanzen im Gehororgan des durch Arzneimittel vergifteten Meerschweinchens. 111. Mitteilung: iiber die Fettsubstanz im entziindeten Gehororgan des Meerschweinchens, kurze Ausziige aus der Zeitschrift fur Oto- Rhino- und Laryngologie (Organ der Japan. O.R.L. Gesellschaft) Band 41. Tokyo, Japan.

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Osol, A. & Pratt, R. 1973. The United States Dispensatory, 27th Ed. (ed. A. R. Gennaro). J . B. Lippincott Company, Philadelphia, USA. Ozeni, J. 1937. Vergleichende Studien iiber die Storungen des Gehororgans durch verschiedene Arzneimittel. Z Oto- Rhino- und Laryngologie (Organ der Japan. O.R.L. Gesellschaft) Band 43. Tokyo, Japan. Quick, C . A. & Duvall, A. J. 1970. Early changes in the cochlear duct from ethacrynic acid: an electronmicroscopic evaluation. Laryngoscope 80, 954. Rollin, H. 1940. Zur Kenntnis des Labyrinthhydrops und des durch ihn bedingten Meniere. Z Hals Nus Ohrenheilkd 31, 73. Riiedi, L. 1951. Some animal experimental findings on the functions of the inner ear. The Scientific Papers of the American Otological Society 88, 993. Schuknecht, H . F. 1955. Presbyacusis. Laryngoscope 65, 402. Schuknecht, H. F . & Igarashi, M. 1964. Pathology of slowly progressive sensori-neural deafness. Trans Am Acad Ophthalmol Otolaryngol68, 222. Smith, C. A . 1957. Structure of the stria vascularis and the spiral prominence. Ann Otol Rhinol Laryngol66, 521. Spoendlin, H . 1967. Vascular stria, In Submicroscopic structure of the inner ear (Red. S . lurato). Pergamon Press, London. Tasaki, I . & Spyropoulous, C. S. 1959. Stria vascularis as source of endocochlear potential. J Neurophysiol 22, 149. Wersall, J. 1956. Studies on the structure and innervation of the cristae ampullares in the guinea pig. Acta Otolaryngol (Stockh), Suppl. 126. 1. Matti Anniko, M.D. Dept. of Otolaryngology Huddinge Sjukhus S-141 86 Huddinge Sweden

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Damage to the stria vascularis in the guinea pig by acute atoxyl intoxication.

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