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PubMed1975

Control of the microcirculation of the inner ear.

In general, many similarities are seen between cerebral blood flow and cochlear blood flow in response to vasodilating drugs. Cochlear vessels appear to be weakly controlled by the adrenergic nervous system. Cholinergic agents dilate cochlear vessels, although the vasodilation in the cochlea does not necessarily cause an increase in cochlear blood flow because of the associated hypotension. The effect on the systemic circulation is too profound to make these agents clinically useful. Papaverine, dipyridamole, amyl nitrite, and the plasma kinins produce transient increases in cochlear blood flow. Ten per cent carbon dioxide and 90 per cent oxygen product progressive vasodilation as long as the mixture is inhaled. Hydralazine produces too profound an effect on systemic blood pressure. Histamine and betahistine increase cochlear blood flow but only in doses that produce bronchiospasm in the guinea pig. Nicotinic acid and nicotinyl tartrate have no effect on cochlear blood flow. If one considers safety and efficacy as well as patient tolerance, papaverine appears to be the drug of choice for increasing cochlear blood flow clinically. Histamine and betahistine appear to be acceptable alternatives. Betahistine is no longer available for clinical use because of the failure to demonstrate clinical efficacy of therapy.

Cochlea↗
PubMedDate not supplied

Color threshold and ratio of S100 beta, MAP5, NF68/200, GABA & GAD. I. Distribution in inner ear afferents.

Afferents of chick embryos (Gallus domesticus) VIIIth nerve were examined at E3, E6, E9, E13, El7, and hatching (NH) for anti-S100 beta, anti-MAP5, anti-GABA, anti-GAD and anti-NF68/200 stain. Different ages were processed together to determine if the distribution of these antibodies changed during synaptogenesis and myelination. Color thresholding showed that saturation of pixels changed for S100 beta only 5%, for NF68/200 10%, and for MAP5, 10%, between E9-NH. Color ratio of NF68/200 over MAP5 was 1.00 at E13 and 0.25 at E16 and NH. S100 beta, GABA and GAD were co-expressed on nerve endings at the edge of the maculae and center of the cristae, whereas hair cells in the center of the maculae expressed either S100 beta or GABA, but not both. S100 beta/NF68/200 shared antigenic sites on the chalices, but NF68/200 expression was higher than S100 beta in the chalices at hatching. MAP5 was expressed in more neurons than NF68/200 at E11, whereas NF68/200 was more abundant than MAP5 at hatching. The results suggest that: 1) the immunoexpression of these neuronal proteins is modulated concomitantly with the establishment of afferent synapses and myelination; 2) S100 beta may serve a neurotrophic function in the chalices where it is co-expressed with the neurotransmitter GABA and its synthesizing enzyme GAD.

Animals↗
PubMed2001

Delayed inner ear maturation and neuronal loss in postnatal Igf-1-deficient mice.

Insulin-like growth factor-1 (IGF-1) has been shown to play a key role during embryonic and postnatal development of the CNS, but its effect on a sensory organ has not been studied in vivo. Therefore, we examined cochlear growth, differentiation, and maturation in Igf-1 gene knock-out mice at postnatal days 5 (P5), P8, and P20 by using stereological methods and immunohistochemistry. Mutant mice showed reduction in size of the cochlea and cochlear ganglion. An immature tectorial membrane and a significant decrease in the number and size of auditory neurons were also evident at P20. IGF-1-deficient cochlear neurons showed increased caspase-3-mediated apoptosis, along with aberrant expression of the early neural markers nestin and Islet 1/2. Cochlear ganglion and fibers innervating the sensory cells of the organ of Corti presented decreased levels of neurofilament and myelin P(0) in P20 mouse mutants. In addition, an abnormal synaptophysin expression in the somata of cochlear ganglion neurons and sensory hair cells suggested the persistence of an immature pattern of synapses distribution in the organ of Corti of these animals. These results demonstrate that lack of IGF-1 in mice severely affects postnatal survival, differentiation, and maturation of the cochlear ganglion cells and causes abnormal innervation of the sensory cells in the organ of Corti.

Aging↗
PubMedDate not supplied

[Congenital malformation of the inner ear and repeated meningitis. Anatomo-clinical considerations illustrated by a case].

The atuhors analyze the case of a three-year-old child suffering from an abnormal condition of the left internal ear, revealed by copious discharge of cerebro-spinal fluid at the onset of 5 attacks of meningitis. A direct approach to the plate and the bony and aponeurotic contents of the oval fossa made it possible to seal this off and this was checked surgically eighteen months later. On this occasion a general survey was carried out into the usual circumstances in which such a discovery is made, pathological concepts and treatment for these accidents. It would appear that unusual permeability may be found either in the internal auditory meatus or in the cochlear aqueduct. Therapeutic procedure depends on circumstances. Blocking the oval fossa is not always effective and should be reserved for cases in which abnormalities impair function. Choice between blocking the internal auditory meatus and eradication of the cochlear aqueduct depends to some extent on the information supplied by tomography, but more on the pathogenetic conclusions reached.

Cerebrospinal Fluid Otorrhea↗
PubMed2000

[Effects of microcirculatory disorders of inner ear on blood-labyrinth barrier permeability in guinea pigs].

OBJECTIVE: To study the changes of blood-labyrinth barrier permeability during cochlea microcirculatory disorders in guinea pigs. METHODS: Using modified method of Evan's blue fluorescence, the changes of permeability of blood-labyrinth barrier were observed in the animal model of cochlea microcirculatory disorders which was induced by photochemical reaction. RESULTS: Amount of Evan's blue passing through the blood-labyrinth barrier was (1.709 +/- 0.769) microgram per guinea pig after 2 hours and (2.849 +/- 0.653) microgram per guinea pig after 4 hours when the cochlea was in microcirculatory disorder. CONCLUSION: The results indicated that the permeability of blood-labyrinth barrier increased when cochlea microcirculatory disorders occurred and the increase of blood-labyrinth barrier permeability may be one of the important mechanisms which causes the cochlear ischemic lesions.

Animals↗