Causation and prevention of sensorineural hearing loss after ear surgery. In: Sensorineural hearing loss.
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The influence of various toxic substances and of drugs with ototoxic side effects upon energy generation, energy utilization, and membrane processes of the cochlea were studied. None of the drugs tested interfered with energy generation to as great an extent as did anoxia or cyanide and 2,4-dinitrophenol. Ouabain produced a pronounced interference with energy utilization of the stria vascularis. The "loop" diuretics ethacrynic acid and furosemide produced a reduction of energy utilization of a lesser degree than did ouabain. The "loop" diuretics do not seem to exert their toxic action upon strial Na+K+-ATPase, but may act by interfering with strial adenylate cyclase. Aminoglycoside antibiotics and diuretic and nondiuretic mercurials seem to exert their primary noxious action upon cochlear function by interfering with membrane processes of the structures bounding the cochlear duct.
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The effects of artificial perilymph at various pH levels and osmolarities on the endocochlear potential (EP) were investigated in a guinea pig model. In 47 ears, the mean EP was 74.5 +/- 0.5 mV in the second turn of the cochlea before perilymphatic perfusion. The artificial perilymph with a pH ranging from 5 to 9 and tonicity less than 1.25 (osmolarity, 345 mosmol/l) did not alter the EP when testings were recorded for at least 1 h. However, after the start of a perfusion with a pH less than 4, the EP declined gradually but recovered to the pre-perfusion level rapidly when the perfusion was stopped. The artificial perilymph with a pH over 10 decreased the EP considerably but showed no recovery, even after cessation of the perfusion. Tonicity more than 1.35 (osmolarity, 372.6 mosmol/l) also decreased the EP, with this decrease paralleling further increases in the tonicity used. From these data, we have concluded that a perilymph perfusate with a pH from 5 to 9 and an osmolarity less than 350 mosmol/l can be used in animal testing without any noxious effects on the EP.
The endocochlear potential and potassium concentrations in endolymph and perilymph were simultaneously measured in the basal turn of the guinea pig cochlea with double-barreled K+ selective electrodes. The K+ conductance and K+ permeability coefficient of the endolymph-perilymph barrier were calculated from the rate of change of endolymph K+ concentration relative to the K+ electrochemical potential difference recorded during permanent anoxia. When anoxia was induced in guinea pigs treated with kanamycin, the rate of decline of the electrochemical potential difference for K+ between the endolymph and perilymph was reduced when compared to normal guinea pigs. In guinea pigs exposed to broad band noise at 115 dBA for periods from 11-15 days, the rate of decline of the electrochemical potential difference for K+ across the endolymph-perilymph barrier was reduced but not to the extent found in guinea pigs treated with kanamycin. The K+ conductance and K+ permeability coefficient of the endolymph-perilymph barrier showed substantial decreases in noise exposed and kanamycin treated guinea pigs, as compared to normal guinea pigs. The magnitude of decrease of K+ permeability of the endolymph-perilymph barrier by noise or kanamycin was correlated with suppression of the maximum output of the cochlear microphonic.
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The dc potential and ion composition (K+, Na+, and Ca++) in the hair cells of the cochlea were examined using ion-selective microelectrodes. The K+, Na+, and Ca++ concentrations were 124.0 +/- 29.8 mM, 6.9 +/- 4.1 mM, and 1.7 +/- 1.4 microM in the hair cells, respectively. The electrochemical potential gradients for K+, Na+, and Ca++ across the apical membranes of the hair cells were calculated to be 160.0 +/- 29.8 mV, 87.6 +/- 27.0 mV, and 194.4 +/- 35.2 mV, respectively. Those for K+, Na+, and Ca++ across the basolateral membranes of the hair cells were -12.6 +/- 33.3 mV, 126.8 +/- 28.3 mV, and 170.8 +/- 30.1 mV, respectively. These findings were discussed in light of the transport mechanism necessary to maintain the ionic composition of hair cells.
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Endolymphatic hydrops of the nonprogressive type occurs in response to a single traumatic or toxic insult of limited duration and although it may result in permanent deficits in sensorineural function, there is total subsidence of vestibular symptoms. Endolymphatic hydrops of the progressive type, on the other hand, appears to be the result of permanent impairment of endolymph resorption and is caused principally by disorders of the endolymphatic sac. It occurs in Menière's disease, syphilitic labyrinthitis and the delayed hydrops syndrome. In addition to deafness of varying extent, it is characterized by episodic vertigo and sometimes by Hennebert's sign. Histological studies suggest that the acute vertiginous episodes are caused by potassium intoxication following ruptures of the membranous labyrinth and that Hennerbert's sign is caused by vestibular fibrosis.