Ann Otol 85: 1976

EFFECT OF ANESTHESIA ON SUSCEPTIBILITY TO ACOUSTIC TRAUMA MOSHE RUBINSTEIN, M.D. NECHAMA PLUZNIK, M.A. TEL HASHOMER, ISRAEL

SUMMARY - In an effort to ascertain whether differences in susceptibility to noise depend on general condition, awake and anesthetized guinea pigs were given a 4 kHz pure tone overstimulation under identical conditions. Cochlear hair cells were histologically examined four weeks after the noise exposure. The damage was localized in the upper part of the first turn and the lower part of the second turn. One fourth as much damage occurred in the anesthetized group. The distribution of damage in the four rows of sensory cells was different in the two experimental groups. In both groups of animals the damage was localized mainly to the outer hair cells, the first row sustaining the major damage.

The damage induced by acoustic overstimulation is a result of the contribution of three factors: 1) the intensity and frequency of the stimulus; 2) duration and distribution of exposure; and 3) individual susceptibility. Extensive studies were carried out on the first two factors in an effort to correlate the different parameters with the magnitude of the resulting hearing loss. The "damage risk criterion" as an example of such correlation, is true if a large population is considered, but cannot be applied to individuals because of the large differences in susceptibility. Individual differences have also been found in laboratory animals. According to Spoendlin! "there are great variations in susceptibility to acoustic trauma between individual animals, between the ears of one single animal and among neighboring sensory cells." Fosbroke 1830-1831, as cited by Ward- appears to be the first to note individual differences and described this as "original imperfection in the constitution of the ear in structure and function." Conversely, Ward'' advanced the hypothesis that the variable sus-

ceptibility was due to changes in the "internal physiological milieu" associated with the activity of the organism causing the individual susceptibility at a given moment. We observed clinically a group of eight soldiers exposed to noise for more than two hours. Three of them were unconscious, but the remaining five were able to seek some form of protection. Despite such protection, it was found that the labyrinthine damage was greater in the conscious group. This observation, reinforced later by other analogous cases, supported Ward's" momentary physiological state hypothesis and provided the incentive to study this phenomenon experimentally. Our approach was to expose two groups of animals to acoustic overstimulation under identical experimental conditions, one group being anesthetized to simulate the field condition described above. 'We could then ascertain the extent of induced damage caused by the changed physiological state.

From Tel Aviv University Medical School and School for Communication Disorders, Haim Sheba Medical Center, Tel Hashomer, Israel.

276

ANESTHESIA AND ACOUSTIC TRAUMA SOUND ROOM MODEL iae 1202-A

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Fig. 1. Sound room Model lAC 1202A with apparatus set up for sound exposure. METHODS AND MATERIALS

Sixteen 300 - 350g male guinea pigs were randomly divided into two equal groups and exposed to the same acoustic overstimulation. Each animal in one group was anesthetized with 15 mg Nembutal®" injected intraperitoneally and the other group was exposed in normal awake state. Sound stimulus was delivered by an audiometerv" connected to a 50 W amplifier with a power supply, a timer, and a 50 W wide-range loudspeaker. The acoustic intensity was monitored by a precision sound level meter...... connected to an octave band filter......... The noise exposure was done individually for each animal and was performed in a double wall soundproof room, .......... the speaker being fixed near the ceiling (Fig. 1). The animal was held in a restrictive cage, the description of which may be of interest to other investigators. It is a cylinder made from fine metallic mesh, measuring 5 cm in diameter and 17 em in length, the dimensions fitting those of the animals. One end is closed and a removable cover can be clamped to the other end. The cylinder is held by a laboratory stand and is directed towards the loudspeaker. The animal is forced to face the

277

source of sound and the only movement possible is a slight rotation of the head. The microphone measuring the sound pressure level ( SPL ) , is placed under the anterior part of the cage near the animal's head. In order to enhance localization of the induced cochlear damage a 4 kHz pure tone was used as stimulus. In acoustic overstimulation the labyrinthine damage is due to two factors, namely, one being the hair cells hyperactivity, or as mentioned by Spoendlinl "metabolic exhaustion," and the second being the excessive vibrations of the basilar membrane. The stress of this structure was defined by Schuknecht and Tonndorf3 as mass times acceleration per unit area. The two factors overlap in their noxious effect. At low SPL the dominant factor is the hyperactivity of the hair cells and at high SPL the mechanical factor is most important. Spoendlins stated that "from 90-130 dB permanent acoustic traumatic damage mainly of the metabolic type may occur." We chose an intensity of 120 dB SPL for two hours, where most of the damage should be a result of the hair cells metabolic exhaustion. A 2-hour exposure time was decided upon in order to produce evident damage at the intensity used. Longer durations would increase the risk of pulmonary complications in the anesthetized group. Cochleas were extracted from the animals four weeks after the single noise exposure. At this time the degeneration of hair cells was sufficient to allow for visualization. They were fixed in 1% OsO, in 0.IM sodium cacodylate buffer (pH 7.3) and surface preparation was made as described by Engstrom et al.5 They were observed by Nomarski differential interference contrast technique. The damage criterion was extensive impairment to the cilia and specific "scars" caused by an ingrowth of the phalangeal cells where hair cells were missing. One of the anesthetized animals died during noise exposure and one animal from the other group was discarded due to a technical mishap, leaving 14 cochleas for examination in each group. Both ears were examined in each animal. RESULTS AND DISCUSSION

A total number of 84123 hair cells (including damaged cells) were counted in the four rows of the awake group and 846-'39 in the anesthetized group (Table I). There were no significant differ-

.. Abbott Laboratories, South Pasadena, Calif . .... Model 15 CX, Beltone, Chicago, Illinois ...... Type 2203, Bruel & Kjoer Instruments, Inc., Cleveland, Ohio ........ Type 1613, Bruel and Kjoer Instruments, Inc., Cleveland, Ohio .......... Model 1202A, Industrial Acoustics Company, I.N.C., Bronx, New York

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RUBlNSTEIN-PLUZNIK TABLE I DISTRIBUTION OF DAMAGE OVER THE DIFFERENT ROWS OF HAIR CELLS IN THE TWO GROUPS OF ANIMALS Group

of

Animals

Total Counted Cells

Row

Damaged Cells

17862 66261

!He OHC , OHC. OHC.

694 2085 1548 1503

18099 66540

!HC OHC , OHC. ORC,

58 757 296 315

Awake

Anesthetized

IRC - Inner hair cell row. ORC - Outer hair cell rows.

ences in the number of hair cells counted in the various rows of the two groups of animals. A total of approximately 6,000 cells were counted per animal which is 65.5% of the total hair cell population as calculated from Stockwell et al.6 Most of the damage occurred in the upper part of the first turn and lower part of the second turn. This fits Schuknecht's" finding that 4 kHZ is received in the upper part of the first turn in cats. While dissecting this portion of the basilar membrane precautions were taken always to include this area. The data, as summarized (Table II), indicates that anesthetizing the guinea

pigs decreased the damage by a factor of four under controlled identical conditions. The statistical analysis of the data (Table III) showed a few interesting points. The differences between the ears of the same animal and between the animals within the same group was bigger in the awake group, than in the anesthetized group. This could partially be explained by the fact that the awake animal, by rotating the head, could protect one ear. However, Stockwell et a16 have reported strong individual differences of the two ears in response to the same auditory stimulus even in animals restrained in a neck-clamping device.

TABLE II DIFFERENCE IN TOTAL AMOUNT OF DAMAGED CELLS IN THE TWO GROUPS OF ANIMALS Group of Animals

Total Number of Cells in Eaclv Group

Total Number of Damaged Cells in Each Group

Damage °

Awake Anesthetized

84123 84639

5830 1426

6.93 1.68

" Anesthesia decreased the damage by a factor of 4.

%

ANESTHESIA AND ACOUSTIC TRAUMA

279

TABLE III THE EFFECT OF ANESTHESIA ON THE DAMAGED HAIR CELLS DUE TO ACOUSTIC OVERSTIMULATION

Awake

Row

IRC OHC, OHC"

OHC. Total:

SD Between '1oof Damage Ears 3.94 9.47 7.14 6.82 6.93

6.51 6.30 4.26 4.95

Anesthetized SD Between Animals 5.59 5.97 9.05 8.84

Furthermore, taking into consideration the supposition that any movement of the head, however slight, could in some way protect the awake animal and therefore result in less damage, the damage as a whole was proved to be four times greater in the awake group as compared with that incurred in the anesthetized group. The difference between groups was evident for each row of hair cells, even the smallest being significant at the 5% level. Generally, as can be seen from Table I, the damage in the outer hair cell rows (ORC) is much greater than in the inner hair cell rows (IRC ) in both groups. A possible explanation for the different response of the inner hair cell row from the outer ones may depend on differences in structure. The inner row hair cells are completely surrounded and protected by their supporting cells. The hair cells in the outer rows are only partially supported by the phalangeal cells and are immersed in the fluid of space of Nuel; this would afford much less protection from the strong vibrations of the basilar membrane. It has also been suggested by Dallos et a18 that the cells of the inner row are at least 30 dB less sensitive than the outer hair cells, and thus it seems possible that they have a higher damage threshold, resulting in less damage. The displacement of the basilar membrane is

SD Between '1oof Damage Ears 0.34 3.30 1.32 1.57 1.68

Level of Significance

SD Between

Between Groups (~

Animals

0.51 1.49 0.46 0.45

0.73 2.70 1.04 0.96

test)

0.05 0.01

om 0.05

probably greatest near the outer first row of hair cells, thus it is more susceptible to damage. Apart from the great differences in the amount of damage between the two groups as previously mentioned, the different distribution of damage within the four rows of hair cells in each group requires some comment. Examining the number of damaged cells in the different rows, one can see that for every single IRC missing there are three in the ORC! in the awake group and 13 in the anesthetized one (Fig. II). The same can be seen in Table III where the number of damaged cells appear as percentages of the total counted cells. awake group

IHC

[Q [Q

OHC z

CD 0

OHC 3

[EJ

OHC I

anesthetized graup

13

J

I 54

I

Fig. 2. Difference in the ratio of damage between inner outer hair cells in the two groups. In the awake group for every single IHC damaged there are three in the first row of the OHC, two in the second and 2.2 in the third. However, in the anesthetized group, for every single IRC there are 13 in the OHC in the first row, 5 in the second, and 5.4 in the third row.

It is peculiar that in spite of the greater damage found in the awake animals, the contribution of the ORC! is

280

RUBINSTEIN-PLUZNIK

less important in this group than in the anesthetized one. It is tempting to link it with another unexplained finding, namely the hyperactivity of the efferent terminal knobs of the ORC described in acoustic overstimulation by Babel, et al,9 and to assume that possible protection is given to the ORC by the inhibitory system. Statistical analysis using Kempthorne's!" formula, however, did not confirm that the difference in distribution of damage between the two groups is significant. We are presently attempting to substantiate this finding using various approaches.

CONCLUSION

Individual susceptibility is an important factor in determining the extent of labyrinthine damage induced by acoustic overstimulation. The present study supports Ward's" hypothesis that the difference in susceptibility to noise is due to changes in the "internal physiological milieu." By changing the metabolic activity of animals which are exposed to noise, one can expect a change in the extent of damage caused to the cochlea. We do not have sufficient statistical evidence to establish whether the efferent activity plays a role in the induced labyrinthine damage.

REFERENCES 1. Spoendlin H: Primary structural changes in the organ of corti after acoustic overstimulation. Otolaryngo171:166-176, 1971

Patterns of hair cell damage after intense auditory stimulation. Ann Otol Rhinol Laryngol 78:1144-1167, 1969

2. Ward WD: Susceptibility to auditory fatigue. Contribution to sensory physiology 3: 191-226, 1968

7. Schuknecht HF: Techniques for study of cochlear function and pathology in experimental animals. Arch OtolaryngoI58:377-397, 1953

3. Schuknecht HF, Tonndorf J: Acoustic trauma of the cochlea from ear surgery. Laryngoscope 70:479-505, 1960 4. Spoendlin H, Brun JP: Relation of structural damage to exposure time and intensity in acoustic trauma. Acta Otolaryngol (Stockh ) 75 :220-226, 1973 5. Engstrom H, Ades HW, Hawkins JE, Jr: Cytoarchitecture of the organ of Corti. Acta Otolaryngol [Suppl] (Stockh) 188:9299, 1964 6. Stockwell CW, Ades HW, Engstrom H:

8. Dallos P, Cheatham MA, Ferraro J: Cochlea mechanics, nonlinearities, and cochlear potentials. J Acoust Soc Am 55, No.3: 597-605, 1974 9. Babel J, Bischoff A, Spoendlin H: Ultrastructure of the Peripheral Nervous System and Sense Organs. Bischoff (ed), Stuttgart, Georg Thieme Verlag, 1970, pp 184 and 186 10. Kempthorne 0: The Design and Analysis of Experiments. New York, John Wiley & Sons, 1952, p 156

REpRINTS: M09he Rubinstein, M.D., Tel Aviv University Medical School and School for Communication Disorders, Haim Sheba Medical Center, Tel Hashomer, Israel.

MODERN LARYNGOSCOPY AND BRONCHOESOPHAGOSCOPY The Division of Head and Neck Surgery of the UCLA School of Medicine will conduct intensive continuing education courses in the techniques of flexible, tube end and telescopic endoscopy. This theoretical and practical course will be held June 12-13, 1976 and November 27-28, 1976. Registration limited to 24. For further information write: Paul H. Ward, M.D., Division of Head and Neck Surgery, UCLA, School of Medicine, Los Angeles, Calif. 90024.

Effect of anesthesia on susceptibility to acoustic trauma.

In an effort to ascertain whether differences in susceptibility to noise depend on general condition, awake and anesthetized guinea pigs were given a ...
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