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A Viberg

Publications and source records attributed to A Viberg.

8 recordsLinked to original sources
PubMed2000

Blood-perilymph barrier and ototoxicity: an in vivo study in the rat.

Cisplatin and gentamicin are two ototoxicants that are supposed to be transported by the paracellar route, i.e. via cellular junctions, to the perilymphatic compartment. This study was initiated to test the hypothesis that susceptive variation of individuals to ototoxic drugs may be explained by variability in transport properties. The transport of radioactive mannitol through the blood-perilymph barrier was correlated in vivo with the acute effect of cisplatin and gentamicin on auditory function. Transport of radioactive mannitol across the blood-perilymph barrier was monitored by sampling of scala vestibuli perilymph at 60 and 120 min after an intravenous infusion of the tracer to nephrectomized Long Evans rats. Counting of hair cell loss was performed in the animals receiving 16 mg/kg body weight cisplatin. The transport of radioactive mannitol across the blood-perilymph barrier did not correlate with the ototoxic effect of cisplatin, evaluated as changes in the auditory-evoked brainstem response thresholds or loss of outer hair cells. The results provide evidence that the barrier function is not involved in the interindividual variability of the ototoxic effect of cisplatin. Furthermore, it can be postulated that neither cisplatin nor gentamicin induce a disruption of endothelial cell junction stability in the inner ear.

Animals↗
PubMed1999

Medial olivocochlear efferent terminals are protected by sound conditioning.

Synaptophysin immunoreactivity was used as a marker for the olivocochlear efferent system that innervates the outer hair cells of the cochlea. An intense noise exposure at either 6.3 kHz or 1.0 kHz caused a significant reduction in anti-synaptophysin immunoreactivity within the 8-6 mm or 14-11 mm distance from the round window, respectively. In the region of the main lesion, the reduction in synaptophysin immunoreactivity for both the 6.3 and 1.0 kHz exposures correlated well with outer hair cell loss. In regions peripheral to the main lesion, some remnants of efferent nerve endings could remain even when their associated outer hair cells were missing. Pre-treatment with a low level sound conditioner (either at 6.3 tone or 1.0 kHz) effectively reduced the efferent and outer hair cell pathology induced by the 6.3 and 1.0 kHz intense noise exposures, respectively. The results demonstrate the feasibility of using anti-synaptophysin immunoreactivity as an effective means of quantifying pathological alterations to the medial cochlear efferent terminals throughout the cochlea. Furthermore, the results show that sound conditioning significantly reduces damage to the efferent terminals.

Acoustic Stimulation↗
PubMed1995

Extra inner hair cells: prevalence and noise susceptibility.

A total of 39 cochleae, 10 non-exposed and 29 noise exposed cochleae, were analyzed in a scanning electronmicroscope. Inner hair cells (IHCs) localized on the modiolar side of the ordinary row of IHCs were described. The mean number of such extra IHCs was 11 per cochlea both for non-exposed and exposed ears, ranging from 0-37. They showed a bimodal distribution with a maximum number at apex and 6-9 mm from apex. The dimension of the cuticular plate was slightly but significantly larger than for the ordinary IHCs. The extra IHCs suffered significantly less damage to their stereocilia than the ordinary IHCs after short-term high-level noise exposure. There was a significant negative correlation between the number of extra IHCs and the size of the post exposure permanent threshold shift. There was no evidence of postexposure generation of extra IHCs in or near the region of hair cell damage. It was concluded that extra IHCs normally occur in rabbits and that they are less susceptible to noise trauma than ordinary IHCs. The negative correlation between extra IHC occurrence and noise susceptibility needs further analysis.

Acoustic Stimulation↗
PubMed1987

Age-related hair cell loss in spontaneously hypertensive and normotensive rats.

In the spontaneously hypertensive (SH) rat, a hereditary form of hypertension and widespread vascular abnormalities develop. In the present study the inner ear degeneration pattern in SH and normotensive (N) rats not exposed to noise was investigated and correlated with frequency-specific auditory brainstem response (ABR) thresholds. Rats of both strains were found to have a spontaneous loss of apical hair cells, but this was slightly more pronounced in SH. In SH rats, but not in those of the N strain, there was an age-related progressive loss of outer hair cells in the region 3-5 mm from the stapes, and a slight additional loss at the most basal end. According to available frequency maps, the hair cell loss should correspond to hearing loss between 6 and 24 kHz. In the SH rats hearing loss was not observed in the whole of this range, only at 16 and 20 kHz. It cannot be determined to what extent the localized spontaneous loss of hair cells is caused by vascular factors and what other mechanisms are involved, but vascular factors probably only play a minor role.

Age Factors↗
PubMed1980

Role of heating in non-invasive blood pressure measurements in rats.

The "tail-cuff" technique for indirect blood pressure measurements was standardized, with respect to heating, in experiments on 47 adult Sprague-Dawley rats. The direct, intra-arterial, and the indirect blood pressures were simultaneously obtained. Pulse volume was recorded from the tail by a non-invasive technique, and was controlled by gradual application of heat. It was found that pulse volume and body temperature were poorly related. A stable relation existed, however, between the error in the indirect blood pressure recordings and the pulse volume. The error was minimized, provided that the heating was adjusted to induce a pulse volume of at least 25% of the maximum obtainable value. It was suggested that the validity of the indirect blood pressure recording could be improved, if heat application was regulated on the basis of observations of pulse volume in the tail instead of ambient temperature or body temperature. Errors due to excessive vasoconstriction, or discomfort due to overheating could thereby be minimized.

Animals↗
PubMedDate not supplied

Peripheral cell loss related to calcium binding protein immunocytochemistry in the dorsal cochlear nucleus in CBA/CaJ mice during aging.

The influence of cochlear hair cell and spiral ganglia neuron loss on calcium binding protein immunoreactivity (calretinin, parvalbumin and calbindin) in the dorsal and posteroventral cochlear nuclei (DCN and PVCN) in CBA/CaJ (CBA) mice during aging (1-39 months) was determined. Since calcium binding proteins have buffering properties against calcium overload, they may have a protective role during aging. It is shown that the percentage of calretinin- and parvalbumin-immunopositive neurons in the DCN showed a statistically significant positive correlation with inner hair cell loss, outer hair cell loss, and spiral ganglion cell loss. A correlation was also found between aging and the auditory periphery, and calcium binding proteins in the DCN. These findings imply that the pathophysiological state of the auditory periphery may influence the neuronal homeostasis in the dorsal cochlear nucleus.

Aging↗
PubMedDate not supplied

Succinic dehydrogenase histochemistry as an early marker for hair cell pathology.

Density measurements of succinic dehydrogenase (SDH) activity were obtained from the inner and outer hair cells on surface preparations obtained from the guinea pig cochlea. Guinea pigs were exposed to noise (3.85 kHz, 120 dB SPL, 22.5 min) and sacrificed 0, 4 or 24 h after the exposure. By 4 h after exposure, the first- and second-row outer hair cells already demonstrated an altered SDH activity. By 24 h after exposure, a significant decrease in SDH staining in both the inner and outer hair cells at a distance of 10-12 mm from the cochlear apex was demonstrated. After a 1-month recovery period, scanning electron microscopy confirmed the main lesion site to be at a distance of 10-12 mm. In addition, Hensen's cells (supporting cells) at a distance of 10-12 mm from the apex were intensely stained by SDH after noise exposure, indicating an increase in oxidative metabolism. SDH staining in the Hensen's cells from the unexposed cochleae was not found. In conclusion, our findings suggest that the early use of SDH histochemistry can predict later permanent damage to the organ of Corti.

Animals↗