Influence of weaning strategy on behavior, humoral indicators of stress, growth, and carcass characteristics.

Weaning is one of the most stressful events a calf experiences in our current beef production system. Its effects may include reduced feed intake, increased activity, slower growth, and increased susceptibility to disease. This study was designed to evaluate weaning after a 7-d placement of nose flaps at 7 mo (N, n = 40) and delaying weaning by 49 d relative to 7-mo weaning (D, n = 39) as alternatives to the industry standard; abrupt weaning at 7 mo of age (A, n = 39). The 4-yr trial utilized Angus and Angus X Senepol steer calves. Calves were randomly assigned to weaning strategy after being stratified by dam parity (heifer/cow), hair coat phenotype (normal/slick), and body weight. Behavioral observations were made on five steers per strategy group per year over the weeks surrounding weaning. Activity levels were determined by accelerometers worn on neck collars. Blood samples were obtained from the observed cattle during the last 2 yr to determine haptoglobin and cortisol concentration. Once weaned, the steers were followed through finishing and carcass characteristics obtained at harvest. Twelve of 38 steers in the N group had sores in their nostrils from the nose flaps when the flaps were removed at weaning of A/N (237 ± 3 d of age). The A and D calves were more active than N calves in the first 2 to 3 d after weaning but settled down to similar activity levels to N by the day 4. The A and D groups were more vocal than N during the same time frame. Cortisol and haptoglobin remained within normal reference ranges. Average daily body weight gain (ADG) was greater for D than A, who in turn had greater ADG than N during the first 42 d after A and N calves were weaned (0.69, 0.54, and 0.37 kg/d for D, A, and N, respectively; P < 0.01). All treatment groups graded Low Choice at harvest and exhibited similar efficiency of gain during growth and finishing (P > 0.2). Based on ADG during the 42 d after weaning, we recommend delaying weaning when available pasture and cow body condition support this strategy. When conditions do not permit delayed weaning, abrupt weaning may be the next viable option based on animal welfare concerns and increased handling to place and remove the flaps. Nose flaps reduced vocalization at weaning but resulted in less postweaning ADG. Based on our data, we suggest that abrupt weaning under the conditions of this study, is less stressful than we perceive it to be, based on calf behavior.

Enhancing the adoption of stockpiling tall fescue and managed grazing.

One of the primary goals of extension is to encourage and support adoption of improved technologies. Managed grazing and stockpiling forage are two such technologies. The goal of this project was to encourage adoption of these practices by providing on-farm demonstrations of the technologies. We also collected forage and soil data and held workshops at each of the demonstration sites. Host producers were selected, given a basic kit of temporary fencing supplies for use during the demonstration, and instructed on their proper use during the winter stockpiling season. Forage yield and quality data were collected and soil tests made to show the economic advantages of proper fertilization and grazing fresh forage in contrast to feeding stored forage and concentrate. The nutritive value of the forage stockpiled in September through November (67% total digestible nutrients [TDN] and 14% crude protein, CP) exceeded the needs of the cattle and was greater than the nutrient content of hay present on the farms (59% TDN and 11% CP, P < 0.01). The mean quantity of available forage (2,856 ± 164 kg dry matter per hectare) provided an average of 260 (±81.8) standard cow (545 kg) grazing days per hectare of stockpiled forage. Taking into account the higher nutritive value of the fresh forage when compared with hay and the savings of time and equipment costs by grazing, we estimated that grazing stockpiled forage saved $1.28 per standard cow per day. The grazing management skills gained during this project and the temporary fencing technology were adopted by 93% of the demonstration farms that responded to our follow-up survey (78% of demonstration sites), and the area managed with these technologies increased on these sites more than 350%. Having the hosts share personal experiences played an important role in encouraging their peers to adopt the technologies.

The neuronal basis of long-term sensorimotor learning.

The brain has a remarkable ability to learn and adjust behavior. For instance, the brain can adjust muscle activation to cope with changes in the environment. However, the neuronal mechanisms behind this adaptation are not clear. To address this fundamental question, this study examines the neuronal basis of long-term sensorimotor learning by recording neuronal activity in the primary motor cortex of monkeys during a long-term adaptation to a force-field perturbation. For 5 consecutive days, the same perturbation was applied to the monkey's hand when reaching to a single target, whereas movements to all other targets were not perturbed. The gradual improvement in performance over these 5 days was correlated to the evolvement in the population neuronal signal, with two timescales of changes in single-cell activity. Specifically, one subgroup of cells showed a relatively fast increase in activity, whereas the other showed a gradual, slower decrease. These adapted patterns of neuronal activity did not involve changes in directional tuning of single cells, suggesting that adaptation was the result of adjustments of the required motor plan by a population of neurons rather than changes in single-cell properties. Furthermore, generalization was mostly expressed in the direction of the required compensatory force during adaptation. Altogether, the neuronal activity and its generalization accord with the adapted motor plan.

Furosemide administered before noise exposure can protect the ear.

OBJECTIVES: We assessed the effect of furosemide administration on noise-induced hearing loss. This drug reversibly elevates the auditory threshold by inducing a temporary reduction of the endocochlear potential and thereby suppresses the cochlear amplifier and active cochlear mechanics. METHODS: Mice were given a single injection of furosemide 30 minutes before exposure to 113 dB sound pressure level broadband noise. Control animals received saline solution. Furosemide was administered in other mice after the noise exposure. Auditory threshold shifts were assessed by recording auditory nerve brain stem evoked response (ABR) thresholds to broadband clicks. RESULTS: The mean ABR threshold in the group injected with furosemide and exposed to temporary threshold shift (TTS)-producing noise was elevated by 20.4 +/- 12.3 dB, and that in the saline control group was elevated by 35.4 +/- 18.3 dB (p < 0.02). The mean threshold elevations in the group injected with furosemide and exposed to permanent threshold shift (PTS)-producing noise and in the PTS saline control group were 15.0 +/- 10.3 dB and 27.0 +/- 12.7 dB, respectively (p < 0.01). Similar results were obtained when the PTS was assessed with an 8-kHz tone burst ABR. There was no significant difference in the PTS between mice given a single injection of furosemide and those given saline solution after the noise; this finding shows that furosemide is not acting as an antioxidant. CONCLUSIONS: It appears that reversible hearing threshold elevation as a result of furosemide administration before noise exposure can reduce the TTS and PTS. This finding provides insight into the mechanism of noise-induced hearing loss.

The effect of noise on ears with a hole in the vestibule.

CONCLUSION: A hole in the vestibule of the inner ear leads to augmentation of the hearing loss following noise exposure. Further research is needed to ascertain the mechanism. OBJECTIVES: The possible effects of a hole in the wall of the inner ear at the vestibule on noise-induced hearing loss were assessed. METHODS: The study was conducted on a total of 14 sand rats. Of these 14 animals, 10 underwent baseline auditory nerve and brainstem evoked response (ABR) threshold measurements in each ear separately (insert earphone), opening of middle ear bulla in both ears and drilling of a hole in the vestibule of one inner ear. The other ear was sham-operated. Following immediate re-assessment of ABR threshold, the 10 animals were exposed to 113 dB SPL broadband noise during 4 nights, and 3 days later ABR measurements were repeated. Four additional animals with a hole in one vestibule, not exposed to noise, served as controls. RESULTS: Following noise exposure, ABR thresholds were elevated by 28.5 +/- 9.1 dB in the ears with the hole, and by 15.5 +/- 7.2 dB in the opposite ear without the hole (significant difference, p < 0.003). In the four control ears, ABR threshold was not elevated a week after drilling the hole.

Salicylic acid injection before noise exposure reduces permanent threshold shift.

The permanent threshold shift (PTS) following exposure to intense noise may be due to the noise-induced excessive vibrations in the cochlea or to the generation of elevated levels of reactive oxygen species. Thus, it is possible that the resulting PTS may be reduced if the cochlear amplifier could be temporarily depressed beginningjust before the onset of the noise and continuing during the noise exposure or if antioxidant drugs were administered. These possibilities were assessed in mice by administering a single injection of salicylic acid (an antioxidant drug which also reversibly depresses the motor protein prestin of the cochlear amplifier) just before, and in other mice, just after, 3.5 h of 113-dB SPL broadband noise exposure. The PTS in the mice injected with salicylic acid just before the noise exposure was significantly smaller than that in mice exposed to the same noise without salicylic acid. The PTS in the latter was not significantly different from that in mice who received the drug just after the noise. Thus a single injection of salicylic acid, just before a noise exposure, can protect the ear from a noise-induced hearing loss.

Salicylate ototoxicity and its implications for cochlear microphonic potential generation.

Salicylic acid causes a reversible sensori-neural hearing loss. Its ototoxicity is probably related to its effect on prestin, the motor protein of the outer hair cells. In order to gain further insight into the mechanism and implications of its ototoxicity, auditory nerve brainstem evoked responses, compound action potentials of the auditory nerve, distortion product otoacoustic emissions, and cochlear microphonic potentials (CM) and vestibular evoked potentials were recorded before and after systemic salicylate administration. These responses were depressed, except for the CM and the vestibular evoked potential. This result and additional considerations provide evidence that the extracellularly recorded CM does not represent the summation of intracellular outer hair cell receptor potentials. It is possible that the CM reflects an early stage of mechano-electrical transduction by the outer hair cells, before the activation of the cochlear amplifier and the later stages of transduction.

Mechanism and rate of middle ear fluid absorption.

Several mechanisms have been suggested to explain the clearance of fluids from the middle ear. These include a pumping action through the eustachian tube, mucociliary beating through the tube, outflow of water to the blood due to osmotic gradients and an active Na(+) transport driving water absorption. In order to assess these mechanisms, the middle ear cavity of paralyzed, ventilated (eustachian tube occluded) guinea pigs was filled with fluids varying in osmotic pressure (hypotonic, isotonic, hypertonic) to which a vertical tube was attached. The change in height of fluid in the tube was taken as a measure of changes in middle ear fluid volume. A greater fluid volume reduction was seen with the hypotonic (1/5 saline) solution. A small volume increase was observed with the hypertonic solution. These results provide evidence that in these experimental conditions, water absorption due to osmotic gradients can contribute to middle ear fluid clearance.

The effects of positive and negative middle ear pressures on auditory threshold.

HYPOTHESIS: To assess the effects of positive and negative middle ear pressures on auditory threshold. BACKGROUND: Nonatmospheric middle ear pressures can alter auditory threshold by their effects on tympanic membrane and ossicular chain mobility. METHODS: Experiments were conducted on guinea pigs by inducing alterations in pressure (positive and negative) with a syringe connected to the middle ear bulla cavity, the magnitude of the pressure being assessed with a water manometer. Elevated middle ear fluid pressures were also induced by attaching a saline-filled vertical tube to the saline-filled middle ear. The effect of these altered middle ear air and fluid pressures were assessed by recording auditory nerve-brainstem evoked responses. RESULTS: There was no effect on auditory threshold of positive middle ear air pressures (up to 250 mm H2O). A negative middle ear air pressure of -50 mm H2O induced a significant 9.5-dB threshold elevation, whereas more negative pressures (up to -150 mm H2O) did not induce an additional threshold elevation. Filling the middle ear cavity with saline induced a 10- to 16-dB elevation, whereas additional fluid pressures (up to 200 mm H2O) did not induce further elevations. CONCLUSION: The major factor inducing threshold elevation in serious otitis media is not the alteration in middle ear pressure but rather the reduction in the volume of compressible air in the middle ear by the fluid.

The production of 10-hydroxystearic and 10-ketostearic acids is an alternative route of oleic acid transformation by the ruminal microbiota in cattle.

The formation of hydroxystearic acid (HSA) and ketostearic acid (KSA) from oleic acid transformation has been documented in a variety of microbial species, including several isolated from the rumen of domesticated ruminant species. However, their ruminal production rates have not been established as influenced by fatty acid source. Dosing continuous cultures of mixed ruminal microorganisms with 1-(13C)-oleic acid increased the 13C enrichment of both HSA and KSA at 24 h postdosing, and showed that the majority (96 and 85%, respectively) of the HSA and KSA present in the 24-h samples originated from oleic acid. Several experiments using batch cultures of ruminal microorganisms showed that production of HSA and KSA was directly related to oleic acid input but was not affected by elaidic acid input, and that HSA was further metabolized to KSA but not to other fatty acids. When continuous cultures of ruminal microorganisms were supplemented with soybean oil or canola oil, production of 10-HSA + 10-KSA was related to oleic acid input but not to linoleic acid input. Daily production of 10-HSA + 10-KSA across treatments was 14.4 micromol/100 micromol oleic acid input into the cultures or 31.1 micromol/100 micromol oleic acid net loss. The results of this study quantify the formation of 10-HSA and 10-KSA from oleic acid transformation by ruminal microorganisms, and show that their accumulation in ruminal contents is directly related to the extent of oleic acid input and biotransformation by the rumen microbiota.

Transmission of oto-acoustic emissions within the cochlea.

Oto-acoustic emissions (OAEs) are low intensity sounds which can be recorded in the external ear canal with a sensitive microphone. They are initiated by the activated motility of the outer hair cells which provide mechanical feedback (the cochlear amplifier) to the basilar membrane, enhancing its displacement. Therefore it has been thought that the OAEs are propagated toward the base as a backward mechanical traveling wave along the basilar membrane. Such a wave would be accompanied by pressure differences across the cochlear partition in the closed cochlear system, filled with incompressible fluid. In order to test this OAE propagation mechanism, holes were made in several places in the bony wall of the inner ear, reducing such possible pressure differences. In experiments in which it was possible to avoid damage to the organ of Corti, there was no change in detection thresholds of distortion product OAEs. This result provides further support for the suggestion that oto-acoustic emissions are not propagated as mechanical vibrations backward along the basilar membrane. Instead it is more likely that they are transmitted through the cochlear fluids to the stapes footplate as alternating condensation/ rarefaction fluid pressures.

Mechanism of cochlear excitation at low intensities.

In order to assess the mechanisms of cochlear activation, the cochlear fluids of one cochlea of a guinea-pig (I) were coupled to those of a cochlea of a second guinea-pig (II) by means of a saline-filled narrow bore tube, the ends of which were placed in the fluids around the opened round windows of both cochleae, thus joining the two cochleae from two different animals into a single, larger, unsealed fluid system. In response to air-conducted sound stimulation of cochlea I, auditory nerve-brainstem evoked responses could be recorded in animal II, not only when the coupling tube was filled with saline, but also when it was filled with ultrasound gel (viscosity 100,000 greater than that of water), when there was a very large hole encompassing a relatively large expanse of the cochlear shell of animal I, and even when animal I was no longer alive. The necessary control experiments were performed. Therefore, it is suggested that at low stimulus intensities, the passive, incoming basilar membrane traveling wave may not activate the cochlea. Instead the fluid pressures (condensation/rarefactions) induced in the cochlear fluids by vibrations of the stapes footplate may be adequate to directly activate the outer hair cells, which then generate an active component of basilar membrane displacement.

Quantitative experimental assessment of the factors contributing to hearing loss in serous otitis media.

OBJECTIVE: This study was designed to quantitatively assess the contribution of various factors to the conductive hearing loss in otitis media. BACKGROUND: In the conductive hearing loss seen in cases of serous otitis media, various volumes of fluid of different viscosities along with subatmospheric (negative) pressure are found in the middle ear. METHODS: To evaluate the contribution of each of these factors to hearing loss, various volumes of saline, whole blood, or glycerol were applied to the open middle ear cavity of guinea pigs for short periods of time and auditory function was evaluated by recording the threshold of auditory nerve-brainstem evoked responses. In some of the saline experiments, the bulla cavity was also sealed, allowing a subatmospheric (negative) pressure to develop in the cavity as water was osmotically absorbed because of the gradient in colloid osmotic pressure between saline and blood in the vessels lining the middle ear cavity. In other experiments, a thoracic drainage system was connected to the middle ear cavity to induce desired negative middle ear pressures. RESULTS: The degree of hearing loss increased as larger volumes of fluid were introduced into the middle ear, reaching a maximum of 15 to 16 dB. There was no difference in the degree of hearing loss induced by saline or by fluids with viscosities up to 1,000 times greater than that of water (glycerol). A subatmospheric pressure in the middle ear contributed only a small additional (1-2 dB) threshold elevation. CONCLUSION: The major factor contributing to hearing loss in serous otitis media is the volume of fluid in the middle ear, irrespective of its viscosity. The contribution of negative middle ear pressure is much smaller.

New approach for implantable hearing aids: a feasibility study.

The objective of this study was to test the feasibility of a new kind of implantable hearing device based on a cerebrospinal fluid hydroacoustic pathway by which sound waves are conducted from the dura mater to the inner ear by cerebrospinal fluid. In this prospective animal study, a piezoelectric bimorph was implanted into 2 guinea pigs and 1 dog between the skull bone and the dura at the parietal area. The bimorph was connected transdermally by wires to a click generator. The auditory brain stem response was recorded after stimulation of the piezoelectric device by the click generator. In the 3 animals, the auditory brain stem response could be recorded in response to a stimulus intensity of 135 dB peak equivalent (pe) sound pressure level (SPL; instrument setting), corresponding to 3.8 V activating the device. The auditory brain stem response disappeared during white noise masking, proving that the origin of the response was in the inner ear. The threshold was 125 and 115 dB pe SPL in the 2 guinea pigs and 135 dB pe SPL in the dog (instrument setting). We conclude that transmission of sound waves by a cerebrospinal fluid hydroacoustic pathway to the inner ear is possible. Such a device would have advantages over more traditional implantable hearing devices: it would not be necessary to couple it to the ossicular chain, and it could be used in patients with infected middle ears.

Prior heat acclimation confers protection against noise-induced hearing loss.

Exposure to intense noise stress can cause a permanent noise-induced hearing loss which is thought to be due to elevation of reactive oxygen species in excess of the inherent antioxidant mechanisms of the cell. However, preconditioning to low levels of stress of one type can activate cellular mechanisms leading to the elevation of antioxidant levels so that the cell is then better able to tolerate subsequent severe stress of a different type. This has been called cross-tolerance. Here, we tested this hypothesis by acclimating rats to a moderate heat stress (30 days at 34 degrees C). The rats were exposed to 113 dB SPL noise for 3 days (12 h/day) in three different groups: heat acclimated then noise exposed; noise exposed and then heat acclimated; heat acclimated, then noise exposed and then heat acclimated again. Permanent changes in auditory function--auditory nerve brainstem evoked responses (ABR) and distortion product otoacoustic emissions (DPOAEs)--were evaluated in each of these animals and compared with those in rats exposed to noise only and in control groups of rats. Statistical evaluation of the results showed that when assessed with ABR, each of the heat-acclimated, noise-exposed groups was protected from the noise, even the group that was heat-acclimated after the noise exposure. When assessed with DPOAE, protection was statistically apparent only in the group that was heat acclimated, then exposed to noise, and not in the other groups. Thus, heat acclimation provides protection against permanent noise-induced hearing loss.

Cochlear activation at low sound intensities by a fluid pathway.

In order to assess the mechanisms responsible for cochlear activation at low sound intensities, a semi-circular canal was fenestrated in fat sand rats, and in other experiments a hole was made in the bone over the scala vestibuli of the first turn of the guinea-pig cochlea. Such holes, which expose the cochlear fluids to air, provide a sound pathway out of the cochlea which is of lower impedance than that through the round window. This should attenuate the pressure difference across the cochlear partition and thereby reduce the driving force for the base-to-apex traveling wave along the basilar membrane. The thresholds of the auditory nerve brainstem evoked responses (ABR) and of the cochlear microphonic potentials were not affected in the fenestration experiments. In addition, holes in the scala vestibuli of the first turn did not cause ABR threshold elevations. These results contribute further evidence that at low sound intensities the outer hair cells are probably not activated by a base-to-apex traveling wave along the basilar membrane. Instead it is possible that they are excited directly by the alternating condensation/rarefaction fluid pressures induced by the vibrations of the stapes footplate. The activated outer hair cells would then cause the localized basilar membrane movement.

Further evidence for a fluid pathway during bone conduction auditory stimulation.

This study was designed to evaluate the suggestion that during bone vibrator stimulation on skull bone (bone conduction auditory stimulation), a major connection between the site of the bone vibrator and the inner ear is a fluid pathway. A series of experiments were conducted on pairs of animals (rats or guinea pigs). The cranial cavities of each pair of animals were coupled by means of a saline filled plastic tube sealed into a craniotomy in the skull of each animal. In response to bone conduction click stimulation to the skull bone of animal I, auditory nerve-brainstem evoked responses could be recorded in animal II. Various procedures showed that these responses were initiated in animal II in response to audio-frequency sound pressures generated within the cranial cavity of animal I by the bone conduction stimulation and transferred to the cranial cavity of animal II through the fluid in the plastic tube: they were not responses to air conducted sounds generated by the bone vibrator, were not induced in animal II by vibrations conveyed to it by the plastic tube and were not electrically conducted activity from animal I. Exposing the fluid in the tube to air was not accompanied by any change in threshold. These experiments confirm that during bone conduction stimulation on the skull, audio-frequency sound pressures (alternating condensations and rarefactions) can be conveyed by a fluid pathway to the cochlea and stimulate it.

Effect of an initial noise induced hearing loss on subsequent noise induced hearing loss.

The effect of previous noise induced hearing loss (NIHL) on subsequent NIHL was studied in rats. Three groups of animals were initially exposed to different durations of 113 dB SPL broad band noise (21 days, 3 days or 0 days--unexposed). Their permanent threshold shifts (PTS) from this exposure (PTS1) were evaluated using auditory nerve-brainstem evoked responses (ABR). All the animals were then noise-exposed for an additional 12 days, and the incremental PTS following this exposure (PTS2) was also assessed. The 21 day group showed the greater PTS1 [mean +/- SD: 27.03 +/- 6.78 dB, compared with 11.67 +/- 10.47 dB (3 day group)] and the lowest PTS2 [9.84 +/- 8.19 dB, compared with 13.33 +/- 14.60 dB (3 day group) and 24.04 +/- 12.4 dB (0 day group)]. This group also showed the highest total PTS and lowest SD following the two noise exposures [36.88 +/- 6.29 dB, compared with 25.00 +/- 12.68 dB (3 day group) and 26.35 +/- 11.93 dB (0 day group)]. The results may be explained by the lower effective intensity of the second noise exposure for the animals with a large PTS1 compared to those with little or no NIHL from the first noise exposure.

Semicircular canal fenestration - improvement of bone- but not air-conducted auditory thresholds.

Auditory stimulation can, under certain circumstances, activate the vestibular end organs and this is facilitated by fenestration of a semicircular canal (SCC). Several fenestrated profoundly deaf patients reported improvements in their bone- (BC) but not air-conducted (AC) thresholds. Bone conduction auditory thresholds have been reported to be better than normal in several patients with thinning or absence of bone over a SCC (dehiscence). This phenomenon was carefully studied in the fat sand rat (Psammomys obesus) by recording auditory brainstem evoked responses to BC and AC auditory stimulation, before and after SCC fenestration. Fenestration would be expected to decrease the pressure difference across the cochlear partition, causing a reduction in the amplitude of the classical base to apex input traveling wave, and should therefore lead to an elevation in AC and BC thresholds. Instead, BC thresholds decreased (i.e. improved) following fenestration (by 7.0+/-4.2 dB; P<0.005), while AC thresholds did not change. Thus the cochlea becomes more sensitive to BC, but not AC, stimulation in the presence of a SCC fenestration. This may be due to the removal by the fenestration of a factor impeding BC cochlear responses, or by the addition of a facilitating factor. The result that the SCC fenestration did not affect AC threshold provides support for the concept that at low intensities the outer hair cells are directly activated by components of the fluid pressures surrounding them, which alternate at audio-frequencies. These cochlear fluid audio-frequency pressures are induced by stapes footplate movement and not by a base to apex input traveling wave. The audio-frequency pressures would not be affected by SCC fenestration. The outer hair cell motility thus induced somehow excites the inner hair cells and the auditory nerve fibers. At low intensities the outer hair cell motility causes localized displacement at the appropriate position on the basilar membrane.

The effect of hydrogen peroxide applied to the middle ear on inner ear function.

OBJECTIVES/HYPOTHESIS: The objective was to assess the effect of hydrogen peroxide applied to the middle ear on cochlear and vestibular function. STUDY DESIGN: Prospective animal study. METHODS: Sand rats underwent a right-side total labyrinthectomy, and a polyethylene tube was inserted into the left-side middle ear. Following baseline recordings of vestibular evoked potentials in response to linear acceleration stimuli and auditory brainstem response, each experimental animal received five daily applications of hydrogen peroxide into the left-side middle ear. Two control groups received saline and gentamicin, respectively. Subsequently, recordings were repeated and compared with baseline measurements. RESULTS: Saline administration affected neither vestibular evoked potentials nor auditory brainstem response. In contrast, both responses could not be recorded following gentamicin application. After hydrogen peroxide administration, auditory brainstem response could not be recorded in 25% (3 of 12) of the animals, whereas in the remaining nine animals the average auditory brainstem response threshold was significantly elevated by 55 dB (P =.000002). Linear vestibular evoked potentials could not be recorded in 42% (5 of 12) of the animals. CONCLUSION: It appears that topical hydrogen peroxide adversely affects both cochlear and vestibular function of the sand rat. The study demonstrated the effect of a reactive oxygen species on inner ear function and may be useful in the study of mechanisms responsible for this damage and its protection. Clinically, although an animal model was used in the present study, caution should be exercised when large amounts of hydrogen peroxide are applied to a dry, perforated ear.