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Biomedical subjects

K E Rarey

Publications and source records attributed to K E Rarey.

70 records · Page 4Linked to original sources
PubMed1982

Distribution and significance of norepinephrine in the lateral cochlear wall of pigmented and albino rats.

Picogram quantities of norepinephrine were found in cochlear regions of pigmented and non-pigmented rats. These regions of the cochlea were the modiolus, organ of Corti--osseous spiral lamina and the lateral cochlear wall. The content of norepinephrine in the modiolus and lateral cochlear wall of the pigmented rat was significantly greater than that in areas of the non-pigmented rat. In contrast, there was no statistical difference between the norepinephrine content of the organ of Corti--osseous spiral lamina region of the pigmented rat and that of the albino rat. Since a major difference between the pigmented and albino rats is the presence of melanin-containing melanocytes in the modiolus and lateral cochlear wall region of the pigmented animals, it is possible that norepinephrine is stored in cochlear melanocytes.

Animals↗
PubMed1981

Quantitative evidence for cochlear, non-neuronal norepinephrine.

Endogenous norepinephrine was quantitatively measured in cochlear tissues of pigmented and nonpigmented animals by high-performance liquid chromatography and electrochemical detection. Epinephrine, dopamine and serotonin were not detected. The cochlear norepinephrine content of the pigmented animals was found to be more than double that present in corresponding albinos. Cochlear norepinephrine was only minimally depleted 48 h after surgical removal of the superior cervical ganglion. 12 h after administration of reserpine (5 mg/kg), cochlear norepinephrine was partially depleted. These results indicate that the norepinephrine located in the cochlea is probably not confined entirely to noradrenergic nerve terminals.

Adrenergic Agents↗
PubMed1980

The sensitivity of cochlear albino melanocytes to horseradish peroxidase.

The effects of low concentrations (0.5%--0.0005%) of HRP and varying postperfusion survival times (5.5 hours--15 seconds) on cochlear albino melanocytes were studied by light and electron microscopy. Approximately 50 microliter of differing concentrations of HRP dissolved in artificial perilymph were perfused through the perilymphatic space in 32 albino guinea pigs. Tissues were subsequently treated histochemically to demonstrate HRP reaction product. The results indicate that concentrations of HRP > 0.0005% in combination with postperfusion survival times > 1 hour bring about acute and selective injury to the albino melanocytes; cytoplasmic vacuolization and rupture of cell membranes occurred. The structural integrity of the albino melanocytes appeared unaltered when exposed to 0.0005% concentrations of HRP for less than or equal to 1 hour. An apparently non-toxic 0.0005% concentration of HRP may provide a means of labeling cochlear melanocytes when the effects of other substances on the cells are investigated.

Animals↗
PubMedDate not supplied

Otologic pathophysiology in patients with human immunodeficiency virus.

During the initial phase of clinical diagnosis and treatment of the manifestations of acquired immunodeficiency syndrome, involvement of the ear appeared minor. In the past several years, however, otologic disorders increasingly have been reported in individuals with human immunodeficiency virus (HIV), as well as in retrospective studies of such patients. The otologic data appear quite variable. Functionally, conductive hearing loss, unilateral and bilateral sudden or progressive sensorineural hearing losses, vertigo, and tinnitus have been reported. In addition, tissue responses in each division of the ear have been observed. Based on collective serologic and immunologic diagnostic assays, clinical histories, and temporal bone histopathology, otologic symptoms may not be the direct effect of HIV alone, but rather a combination of the effects of HIV infection coupled with that of opportunistic microorganisms and/or possible ototoxic effects of certain therapeutic agents. It is within this context that otologic findings in this population of subjects will be discussed.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Ototoxicity of toluene in rats.

Toluene is a major industrial solvent and substance of abuse which is ototoxic in rats as shown by both behavioral testing and measurement of brainstem auditory evoked response (BAER) thresholds. The objective of this investigation was to examine the morphological (hair cell loss) and functional (BAER threshold elevations) changes resulting from toluene administration. In the preliminary experiment, 5 male Sprague-Dawley rats were dosed by gavage to 0.5 ml toluene/kg body weight/day in corn oil for 21 days then consecutively to 1.0 ml toluene/kg/day for 21 days. In the main experiment, eight male Sprague-Dawley rats were dosed by gavage for eight weeks with 1.0 ml toluene/kg body weight/day in corn oil. Five and six control rats, respectively, received corn oil only. BAER thresholds were recorded from four toluene-treated and four control rats prior to dosing (main experiment) and from all rats after dosing (both experiments). Loss of outer hair cells occurred in all toluene-treated rats in the middle and basal turns of the organ of Corti, with the greatest loss in the third row and progressively less in the second and first rows. This loss was more severe in toluene-treated rats that demonstrated elevated BAER thresholds in midfrequency regions, typically 2-8 kHz. These experiments demonstrate that auditory changes are associated with cochlear hair cell loss in toluene-treated rats. These ototoxic effects of toluene contrast with those of other known ototoxicants, e.g., aminoglycoside antibiotics, in terms of the position of hair cell lesion in the organ of Corti and in the pattern of hair cell loss.

Animals↗
PubMedDate not supplied

Inner ear changes in the ferret model for Reye's syndrome.

The acute effects of influenza B, aspirin, and hyperammonemia on the inner ear were examined using the ferret model for Reye's syndrome. Histopathologic examination revealed varying degrees of vacuolization in both the sensory and nonsensory endolymphatic tissues of the cochlear and vestibular membranous labyrinth. The secretory epithelial cells of the stria vascularis and the vestibular dark cells appeared to be more severely affected, as demonstrated by the presence of an extensive number of intracytoplasmic vacuoles. The cells of the perilymphatic tissues appeared to be unaltered. Although all neuroepithelial regions of the inner ear appeared to be altered, an unexpected observation was that only the inner hair cells of the organ of Corti were pathologically affected. These results suggest that metabolic and virus-induced derangements may alter inner ear microhomeostasis in patients with Reye's syndrome and may potentially result in loss of hearing in such patients.

Animals↗
PubMedDate not supplied

Intralabyrinthine osteogenesis in Cogan's syndrome.

Temporal bones from a 64-year-old man who had Cogan's syndrome were examined by light microscopy. Although tissues of the middle ear appeared unremarkable, extensive ectopic bone formation was observed bilaterally in the inner ear membranous labyrinth. Such osteogenesis completely obliterated the cochlear compartments apically. Only the scala tympani compartment of the basal cochlear turn remained patent. Ectopic bone tissue was observed also in the vestibular semicircular canals. Marked degeneration of eighth nerve fibers and associated ganglion cells also was observed. To our knowledge, this report represents only the fourth temporal bone findings of Cogan's syndrome and demonstrates a more advanced pathologic state of inner ear pathology than those reported previously.

Adult↗
PubMedDate not supplied

Effect of upper respiratory infection on hearing in the ferret model.

In an effort to develop an adult animal model for acquired viral-induced hearing loss, three groups of mature ferrets were inoculated intranasally with respiratory viruses (influenza A/Port Chalmers, influenza B/Mass, and parainfluenza I), which have been implicated as causative agents in idiopathic sudden hearing loss (ISHL). All ferrets challenged with influenza A/Port Chalmers (A/PC) exhibited clinical signs of infection, but neither of the other two groups exhibited such signs. Conductive and/or sensorineural hearing losses were demonstrated in eight of 15 ferrets challenged with influenza A/PC and four of 10 ferrets in the group challenged with influenza B/Mass by brainstem auditory-evoked responses (BAERs) and acoustic immittance. None of the four ferrets infected with parainfluenza I demonstrated auditory dysfunction. When auditory changes were observed, nasal washes were performed, and tissues of the middle and inner ears were collected for viral assay and morphologic examination. All ferrets demonstrating auditory changes were shown to be infected by isolation of virus from nasal tissues. Virus was isolated from eustachian tube tissue in six of the eight ferrets infected with influenza A/PC, which also demonstrated altered BAERs and one of the four infected with influenza B/Mass, which also had auditory changes. Virus was isolated from the middle ear of two ferrets infected with influenza A/PC and from the inner ear of another two ferrets from the same group. These data suggest that influenza A/PC has a greater effect on auditory function in the ferret model than either influenza B/Mass or parainfluenza I and that the ferret may be an appropriate adult model to examine the etiologic role of viral upper respiratory tract infections in some acquired hearing impairments.

Acoustic Impedance Tests↗
PubMedDate not supplied

Na,K-ATPase subunit isoform expression in the guinea pig endolymphatic sac.

Na,K-ATPase subunit isoform expression was studied by immunocytochemistry in the guinea pig endolymphatic sac, using subunit isoform-specific polyclonal antibodies. Epithelial cells of the guinea pig endolymphatic sac were observed to contain the alpha 1- and beta 2-subunit isoforms, and to a lesser extent the beta 1-subunit isoform, of Na,K-ATPase. The alpha 1- and beta 2-subunit isoforms of Na,K-ATPase have been observed previously in other ion and fluid transporting regions of the membranous labyrinth, e.g., stria vascularis and vestibular dark cells. Combined data indicate that the alpha 1-, beta 2-form of Na,K-ATPase plays a role in the microhomeostasis of endolymph. The alpha 1 beta 2 Na,K-ATPase subunit isoform combination is different from typical ion and fluid transporting tissues, e.g., kidney and colon, and may reflect distinctive characteristics of inner ear Na,K-ATPase.

Animals↗
PubMedDate not supplied

Effects of influenza infection, aspirin, and an arginine-deficient diet on the inner ear in Reye's syndrome.

The individual effects of an influenza B viral infection, aspirin, and an arginine-deficient diet on the inner ear were assessed in the ferret model for Reye's syndrome using both functional and morphological parameters. Auditory brainstem evoked responses recorded from inoculated ferrets revealed threshold elevations and increased latencies during the first 72 hours, but approximated those of control animals by 96 hours. Although there was a mild distention of Reissner's membrane, no pronounced structural alterations in sensory or supporting cells were observed in cochleas from inoculated ferrets. The administration of aspirin appeared to alter neither the functional nor the structural integrity of the cochlea. The presentation of an arginine-deficient diet, creating a hyperammonemic condition, led to both altered auditory evoked responses and vacuolization of cochlear tissues after treated animals had undergone seizures and coma. These data demonstrated that both influenza B and the arginine-deficient diet individually affected the hearing of treated animals. The individual agents did not alter the cochlea as severely as when they were presented in combination. These results suggest that hearing impairment in patients with Reye's syndrome may be a result of potentiation of certain metabolic-altering agents.

Animals↗
PubMedDate not supplied

Recovery and probable persistence of cytomegalovirus in human inner ear fluid without cochlear damage.

Cytomegalovirus (CMV) was recovered from a 5-month-old infant with probable congenital infection. In life, no hearing impairment had been observed. Auditory brain stem evoked responses were bilaterally intact. At necropsy, both temporal bones were morphologically normal, as demonstrated by light and electron microscopy. Sensory hair cells of the organ of Corti appeared intact. Cytomegalovirus was recovered from a mixture of perilymph and endolymph, but not the brain, CSF, or vitreous humor. This appears to be the first report of an individual with an inner ear CMV infection in which neither structural nor functional alterations of the inner ear were apparent. This case also suggests that CMV can persist within the inner ear for prolonged periods following congenital infection.

Atrophy↗
PubMedDate not supplied

A survey of the effects of loop diuretics on the zonulae occludentes of the perilymph-endolymph barrier by freeze fracture.

The acute (30 min) effects of the loop diuretics piretanide, ethacrynic acid, bumetanide, furosemide, and azosemide, and the chronic (8 days) effects of furosemide and bumetanide on the zonulae occludentes (tight junctions) of the perilymph-endolymph barrier in the stria vascularis and in Reissner's membrane of the basal cochlear turns were studied by freeze-fracture. Quantitative analysis of their effects indicated that the structural integrity of the barrier was modified by either as increase or a decrease in the number, depth, and density of the strands of the tight junctions of the strial marginal cells. Only azosemide appeared to modify the tight junctions between the epithelial cells of Reissner's membrane, but it had little effect on the strial junctions. The tight junctions between the basal cells of the stria appeared to be the least affected by the various loop diuretics, although piretanide appeared to increase randomly the intercellular spaces lying between the strands.

Animals↗
PubMedDate not supplied

Functional and morphological changes in experimental endolymphatic hydrops.

Electrocochleograms (ECochG) in response to tone bursts and electronystagmograms (ENG) during sinusoidal rotational stimulation were monitored in guinea pigs equipped with chronically implanted round-window and periocular electrodes before and for as long as 90 days after uni- or bilateral surgical obliteration of the endolymphatic duct. The presence of cochlear and saccular endolymphatic hydrops was verified during microdissection of the inner ear, and cochlear hair cell counts were performed in some of the animals. The results indicate that in surgically-induced endolymphatic hydrops, cochlear and vestibular changes occur similar to those observed clinically in Menière's disease: fluctuant threshold shifts, threshold elevation at low frequencies, sensorineural loss at all frequencies with recruitment, increase in the ratio of summating potential to compound action potential (SP/CAP), asymmetry and recruitment in the ENG, and increased vestibular excitability, with occasional post-rotational and spontaneous nystagmus. Functional changes could not be clearly correlated with those seen by light microscopy, since hair cell loss was confined mainly to the apical coil. The observations indicate that the guinea pig with surgically-induced endolymphatic hydrops can be a useful model of Menière's disease, not only on morphological grounds, but also on the basis of functional changes, which over the relatively short term of observation represent a dysfunction rather than a loss of sensorineural structures.

Animals↗
PubMedDate not supplied

Modulation of the rat stria vascularis in the absence of circulating adrenocorticosteroids.

Structural changes in the cellular morphology of the rat stria vascularis from a standardized region of the basal region and from a standardized region in the apical region of the rat cochlear duct were measured using stereological methods after removal of endogenous levels of adrenal steroids by bilateral adrenalectomy. Although there were some inconsistent and insignificant alterations in the volume density of intermediate and basal cells, a decreased volume density of marginal cells in both the basal region and in the apical region in adrenalectomized (ADX) animals as compared to sham animals was consistent with a concomitant significant increased (p less than or equal to 0.05) volume density of intercellular space as observed in both the basal and apical regions of the stria vascularis of ADX animals. Findings of this study indicate that the strial cells of the stria vascularis react differently and independently in response to the removal of adrenal steroids, and such strial responses occur uniform in both the base and apex.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Ultrastructure of ampullar dark cells in the absence of circulating adrenocorticosteroid hormones.

The morphology of rat ampullar dark cells was studied in the absence of circulating adrenal hormones at two time intervals of 8-14 and 22-28 days. Five morphological parameters of dark cells were quantitatively determined: cell area per baseline length, basolateral membrane surface density, basolateral membrane length per baseline length, volume density of intercellular space and volume density of vacuoles. Significant statistical reduction of basolateral membrane length per baseline length was observed after an absence of circulating adrenal hormones for 8-14 days and 22-28 days compared to sham operated animals that served as control. The basolateral membrane surface density decreased significantly in the animals sacrificed 22-28 days following adrenalectomy compared to sham operated animals. Cell area per baseline length decreased and volume density of vacuoles increased at both time intervals following adrenalectomy; however, these differences were statistically insignificant. The volume density of intercellular space between dark cells was practically constant among the groups. Results of this study are similar to those reported for ion-regulating nephron cells, and support the hypothesis that cells involved in microhomeostasis of vestibular endolymph may at least be partly regulated by adrenal hormones.

Adrenal Cortex Hormones↗