Malate dehydrogenase in postmortem perilymph and endolymph.
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Summary--Aminooxyacetic acid (AOAA; 1 MM) when perfused through the scala tympani of guinea pigs produced a biphasic reduction in the endocochlear potential, together with a shift in the input-output functions of the cochlear microphonics and the compound action potential of the cochlear nerve. Since the ionic (Na+, K+) content of the scala media was not alerted, it appears that such changes did not underlie the reduction recorded in the endocochlear potential. The negative direct current potential recorded in the organ of Corti did not appear to be affected by the drug. Attempts to antagonize the effects of AOAA with pyridoxine failed.
Summary--Because of the topography of the perilymphatic vascular network, the cochlear microcirculation is especially sensitive to the effect of vasoactive substances reaching the perilymphatic space. The cochlear microcirculation is mainly controlled humorally, via the activity of the metarterioles and changes in the flow properties of the blood. Intracochlear histamine reduces the cochlear circulation even more markedly than after intracarotid administration. No systematic effects of parenteral administration of vasoactive substances can be expected on the cochlear circulation. Reversible auditory disorders after stapedectomy may be explicable by the intracochlear release of histamine. The internal release of histamine after sunstroke and cold stress may play a part in sudden dusturbances of hearing.
An experiment was performed on 31 guinea pigs to study the effect of fistulae of the horizontal canal, superior canal, common crus, and utricle on the course of experimentally induced endolymphatic hydrops. The effect of fistulae on corresponding parts of normal ears was also studied in an additional 17 animals. The results indicated a remarkable consistency of healing of the fistulae in both groups of animals. Fistulae had no significant effect on the course of endolymphatic hydrops, irrespective of whether the fistulae were made immediately before or several months after obliteration of the endolymphatic duct or whether a polyethylene strut was introduced into the membranous labyrinth. Once again, the functional significance of the endolymphatic sac was clearly apparent, for ablation of the sac consistently produced severe hydrops and atrophic changes in sensory and neural structures. Assuming that the mechanisms of labyrinth repair in the guinea pig are comparable to the higher mammalian ear, it is apparent that procedures designed to surgically fistulize the membranous labyrinth are of questionable value and are probably not rational therapeutic approaches to the management of Ménière's disease.
An entity of episodic true vertigo of delayed onset following sudden and profound sensorineural hearing loss is described. Data on 12 patients and three case reports are presented. The latency between sudden deafness and the onset of the vertigo varied from 1 to 68 years. The vestibular symptoms are identical to the vestibular symptoms of Ménière's disease, and there is some evidence that endolymphatic hydrops in the previously deafened ear represents at least part of the labyrinthine pathology. Labyrinthectomy in the deaf ear was curative. Tentatively, this entity is best considered a variant of Ménière's disease.