[Qualitative study of the connections of the subarachnoid space with the lymphatic system of the head and neck].
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The review of literature about the inner ear fluid circulation theory was presented. The creation and absorption of fluids were discussed as well as the role of endolymphatic sac in fluid pression regulation.
A volumetric study was made of the endolymphatic compartments of the pars superioris (utricle and semicircular canals). Selected for this comparative study were 15 ears from subjects with unilateral endolymphatic hydrops, 15 contralateral ears, and 15 normal ears. There was an increase in the total volume as well as in the utricular volume. This increase was also correlated with vestibular and auditory symptoms, disclosing a substantial increase in volumes with increasing hearing loss. The magnitude of volume increase correlated inversely with the frequency of vertiginous attacks; no correlation was found with the duration of the disease.
The rate of longitudinal flow of perilymph has been measured using an ionic tracer technique. Spread of the tracer trimethylphenylammonium (TMPA) along the perilymphatic scalae was monitored with ion-selective microelectrodes following injection of a minute bolus (approximately 50 nl) of 150 mM TMPAC1 one turn away. This amount of TMPA had virtually no toxic effect on cochlear function. The spread of tracer by longitudinal volume flow and passive diffusion were separated by comparing tracer movements in both apical and basal directions along the scalae in two groups of animals. Experimental findings were compared with a mathematical model which combined diffusion and volume flow. Our results demonstrated that when electrodes were completely sealed into the cochlea, the rate of longitudinal volume flow in scala tympani was extremely slow, approximately 1.6 nl/min in the apical direction. Longitudinal flow was not detectable in scala vestibuli. When the otic capsule was perforated, flow rates of over 1 microliter/min were recorded in scala tympani, probably as a result of cerebrospinal fluid entry through the cochlear aqueduct. When the cochlea was sealed (with recording electrodes in place) and cerebrospinal fluid pressure was released, there was no significant basally-directed flow of perilymph in scala tympani. These findings support the concept that perilymph composition is maintained by local, cochlear mechanisms which do not involve longitudinal volume flow. They provide strong evidence that perilymph is not secreted in one region and resorbed at a spatially distant site.
The blood-labyrinth barrier is concept that has evolved based on marked difference in chemical composition between perilymph and blood. Studies reported here have been designed to manipulate physiologic, metabolic, and pharmacologic conditions in experimental animals in order to determine the characteristics of this regulatory mechanisms. Tracer studies of uptake of sodium, calcium, and albumin from blood into perilymph showed that these substances penetrate into inner ear fluids quite slowly. Injections of ototoxic substances (kanamycin, furosemide) show limited transport of these agents into perilymph. Administration of an osmotic agent (urea) resulted in a parallel but delayed elevation of perilymph concentration. The possible role of a alteration of blood-labyrinth barrier in inner ear disorders has been discussed.
In rodents at least, the main sources of the perilymph fluid are (1) influx of CSF through the cochlear aqueduct, and (2) blood flow dependent local production within the cochlea. Experimental data are presented that give a ratio of 22:78 percent for those sources. The perilymph production thus derives mainly from the cochlear blood flow. It is concluded that measurements of the perilymph production can be used as indirect measurements of the inner ear blood flow under various experimental conditions. Two experimental examples are referred to.
Fifteen adult rabbits were perfused intrathecally with horseradish peroxidase (HRP) for 20-30 min under conditions that prevented any increase in cerebrospinal fluid (CSF) pressure. Histologic and ultrastructural examination of the cochlea disclosed HRP deposits along the cochlear and vestibular branches of the auditory nerve and beyond their ganglia, in a) epineural and perineural spaces; b) intraneural spaces reaching the membrane of myelinated axons via nodes of Ranvier; and c) extending beyond the epineurium into area lymphatics. HRP was also found in the basilar membrane, along with deposits in the scalae tympani, vestibuli, media and the spiral ligament. The endolymph also received HRP which followed vestibular nerve fibers and penetrated between sustentacular and hair cells of the cristae ampullaris and both maculae. HRP permeated interendothelial spaces lining the modiolus to reach the scala vestibuli lymphatics close to all the above areas were also permeated by HRP, but the inner tunnel was devoid of the marker.
Under normal conditions, the inner ear possesses remarkably stable homeostatic mechanisms for the maintenance of functional integrity of the inner ear fluid. The inner ear fluid maintains its homeostasis by a variety of regulatory mechanisms such as an ion transport system, a blood-labyrinth barrier, and a constant blood supply. Highly regulated transport of ions into and out of the inner ear provides for the maintenance of inner ear fluid composition necessary for auditory transduction. Any disturbance in one of these mechanisms can disrupt homeostasis expressed by ionic, osmotic, or metabolic imbalance between the compartments. Free radicals, stress hormones, noise exposure, and aminoglycoside antibiotics may induce short- and long-term effects on cellular function of the auditory or vestibular system (or both) and serve as a triggering mechanism for abrupt functional disturbances of inner ear fluid ion homeostasis. In this article, we present a comprehensive review of the mechanisms underlying inner ear fluid homeostasis necessary for normal auditory function and factors that can disrupt homeostasis and lead to functional disturbances, namely sensorineural hearing loss, tinnitus, and vertigo.
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