Thin-layer chromatographic investigation of the lipids of inner ear tissues and perilymph of guinea pig.
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The perilymphatic pressure was studied in relation to pressure step variations in the external ear canal and in the middle ear. The transfer of pressure via the ossicular chain reached its limiting value at quite low pressures. When pressure steps were applied directly to the middle ear, there was almost a direct transfer of pressure for positive changes. Nonlinearities were shown between positive and negative pressure steps. The pressure-regulating ability of the inner ear was illustrated by means of calculating the time constants of the pressure transfer curves.
A survey of experimental evidence showing the influence of an increase in potassium concentration in the perilymph on cochlear and vestibular nerve branches is discussed. Informations have indicated that a concentration lower than 20--30 mM produced an increase in action potential frequency in nerve preparations and that a low potassium concentration in animal experiments produced an ipsilateral nystagmus. Increasing the concentration of potassium in the endolymph to values not over the normal endolymph concentration, blocked the conduction of action potentials in the vestibular nerve branches resulting in a reversible contralateral nystagmus. From these results it may be concluded that all objective symptoms of a Ménière attack can be experimentally reproduced by one single factor: the potassium concentration in the perilymph. The known ruptures in the distended walls in a hydrops, with a diffusion of endolymph potassium into the perilymph surrounding the nerve branches to the vestibular and cochlear areas have consequently been assumed to produce the basis for Ménière attacks.
Vertigo in motion sickness forms a clear clinical picture. We can confirm that complex symptoms are due to abnormal stimulations of labyrinth receptors subsequent to simultaneous multi-plane angular accelerations. This labyrinth stimulation originates from Coriolis' complementary accelerations. The seriousness of kinetosis symptoms can vary according to different causes; level of labyrinth stimulation, subject's constitution, psychological and physical conditions and whether or not the subject is accustomed to kinetic stimulations. Space sickness shows similar symptoms and similar psychological mechanisms. Recent space experiences have shown that disturbances due to acceleration sickness vary according to labyrinth receptor adaptability to kinetic stimulations in space. In a clinical and experimental study, we investigated the importance of the spacial plane, in which the head movement occurs, in causing the greatest reactions due to Coriolis' complementary accelerations in man. A close relationship between nystagmic responses and the level of endolymphatic shifting in each canal was observed and studied with the help of mathematical models.
Two cases of rupture of the round window membrane verified by operation are presented. Both cases arose in connection with myringotomy and were presumably caused by a violent force acting directly on the tympanic membrane and the ossicles. This would result in a strong movement of the stapes and an acute change in the perilymph pressure, thereby causing an indirect injury to the round window. Symptoms and treatment are briefly discussed.
The endolymphatic space of pigeons was studied by using double-barrelled electrodes with a potassium liquid ion exchanger. The K+ activity of the endolymph was 155 mM in the cochlea and 133 mM in the ampulla, respectively. Positive DC potential in the cochlea (+14.5 mV) was much lower than in guinea pigs (+80 mV) whereas in the ampulla of pigeons the DC potential (+7.4 mV) was 2 times higher than that of guinea pigs (+3.9 mV). General application of ethacrynic acid in pigeons induced a weak change in DC potential and no typical intercellular edema in the cochlea and ampulla. Local application of ethacrynic acid and ouabain in the cochlea and ampulla of pigeons induced a negative DC potential of between -30 and -40 mV. This negative DC potential was higher than the anoxia-induced negative potential. Short hypoxia during a drug-induced DC potential resulted in a decrease in DC potential above the diffusion potential. Below the diffusion potential additional hypoxia increased the DC potential independent of the cause of intoxication.
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