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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A photochemical reaction between intravenous rose bengal and xenon light was used to induce a selective thrombus in the rat anterior inferior cerebellar artery (AICA). Compound action potentials (CAPs) were recorded by electrocochleography and cochlear blood flow (CBF) was monitored by laser Doppler flowmetry. Photothrombotic occlusion of the AICA caused inner ear ischemia to various degrees with or without alterations of the CAP. With use of this model we investigated the critical range of the CBF for preserving cochlear function, represented by the CAPs induced with 8 kHz half-wave of sinusoid at 100 dB SPL. Results then showed that a CBF range between 26.7% and 42.9% of baseline was somewhat critical for maintenance of cochlear function in an acute phase of ischemia. Pretreatment with heparin significantly delayed thrombotic occlusion of the AICA in a dose-dependent manner. Further use of our model for inner ear ischemia may be useful for studying pathophysiology and pharmacological therapy of cochlear disturbances subsequent to circulatory disorders.
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PMID:An animal model for hearing disturbance due to inner ear ischemia: photochemically induced thrombotic occlusion of the rat anterior inferior cerebellar artery. 821 33

The results of a series of scanning electron microscopical studies were used to construct a model for the vascular pathways in the inner ear. Corrosion cast preparations of the vessels of the inner ear of the adult rat were used in this study. The inner ear is, like a hand, an end organ containing four sense organs (cochlea, saccule, utricle and the cristae ampullaris). All these specific inner ear structures have their own vascular supply. We have developed a blood flow diagram of the inner ear. This model was used for a classification of different types of ischemia in the inner ear and forms a concept for some forms of sensorineural hearing loss and vertigo. Four types of inner ear ischemia are proposed. In type I (a or b) of inner ear ischemia only the vessels of the cochlea are involved resulting in two types of hearing loss without vertigo. Type II is characterized by ischemia of a part of the cochlea and a part of the vestibular system. In type III (a or b) only the vestibular system is involved, while in type IV no blood circulation will be present in the inner ear resulting in total deafness and severe vertigo. Inner ear partition at ultramicroscopical level of these structures may be possible in the future and new imaging techniques will probably support the vascular schematic model presented in this study.
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PMID:Vascular inner ear partition: a concept for some forms of sensorineural hearing loss and vertigo. 955 72

The mechanisms of cochlear hair cell death following exposure to transient inner ear ischemia were investigated in gerbils histologically. The animals were subjected to ischemic insult by occluding both vertebral arteries for 15 min. Hoechst 33342 nuclear staining showed that inner hair cells (IHCs) underwent sporadic degeneration via nuclear condensation, which peaked 12 hours after the ischemia. Furthermore, nuclear DNA fragmentation was noted by the terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP)-biotin nick end labeling method. Transmission electron microscopy revealed morphological changes in the IHCs characteristic of apoptosis, including karyopyknosis, chromatin condensation. These findings suggest that apoptotic cell death is the major process in hair cell degeneration in this animal model.
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PMID:Apoptotic hair cell death after transient cochlear ischemia in gerbils. 1249 49

Ischemia can contribute to the inner ear pathology and hearing loss. To determine the susceptibility of inner and outer hair cells (IHCs/OHCs) to ischemic and post-ischemic period, we used organotypic cultures of the organ of Corti isolated from P3 rats as an in vitro model of inner ear ischemia (oxygen-glucose deprivation, OGD). We identified the hair cells (HCs) by phalloidin staining. The cells with damaged cellular membrane integrity were identified by propidium iodide (PI)-exclusion assay. The cells with fragmented chromosomal DNA were detected by TUNEL assay. Organotypic cultures were subjected to a mild (3 h duration) or severe (4 h duration) OGD, followed by a recovery period of 21 h and 20 h, respectively. Mild OGD induced a loss of 10-20% HCs, whereas severe OGD induced loss of 35% HCs. We confirmed that OHCs are less vulnerable to OGD than IHCs. Of all missing OHCs, 80-90% was lost during the OGD period and 10-20% during the recovery period. In contrast, the loss of IHCs was equal during both experimental periods. The OGD period was mainly associated with PI-positive nuclei. TUNEL-positive nuclei were a minor fraction during the OGD period and increased during the recovery period, indicating the progression of DNA fragmentation. Our results implicate a differential susceptibility of IHCs and OHCs during and after ischemia-like insult, which may be of therapeutic consequence.
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PMID:Differential vulnerability of outer and inner hair cells during and after oxygen-glucose deprivation in organotypic cultures of newborn rats. 1909 32