Biomedical subjects

Shigeki Tsuji

Publications and source records attributed to Shigeki Tsuji.

10 recordsLinked to original sources

PubMed2006

Successful treatment of eosinophilic otitis media using ramatroban: report of two cases.

OBJECTIVE: The pathogenesis of eosinophilic otitis media is not yet fully understood. The purpose of this paper is to describe the clinical course of our two patients with eosinophilic otitis media and to discuss the pathogenesis and treatment of this intractable condition. METHODS: Two cases of eosinophilic otitis media were treated with ramatroban. RESULTS: The middle ear effusion has been well controlled in both patients for more than 1 year with minimal corticosteroid therapy. CONCLUSIONS: Our experience suggests that the pathogenesis of eosinophilic otitis media is related to the pharmaceutical effects of ramatroban, i.e., inhibition of the thromboxane A2 receptor (TP) and the chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2).

Administration, Topical↗

PubMed2006

The effects of tempol, 3-aminobenzamide and nitric oxide synthase inhibitors on acoustic injury of the mouse cochlea.

Oxygen free radicals have been implicated in the pathogenesis of acoustic injury of the cochlea. The purpose of this study was to evaluate the effects of tempol (a superoxide anion scavenger), 3-aminobenzamide (a poly (ADP-ribose) synthetase (PARS) inhibitor), N-nitro-l-arginine (a non-selective nitric oxide synthase (NOS) inhibitor), 7-nitroindazole (a selective neuronal NOS inhibitor) and aminoguanidine (a selective inducible NOS inhibitor) on acoustic injury. Mice were exposed to a 4 kHz pure tone of 110-128 dB SPL for 4h. Tempol, 3-aminobenzamide or N-nitro-l-arginine was intraperitoneally administered immediately before the onset of acoustic overexposure, while 7-nitroindazole or aminoguanidine was intraperitoneally administered every 12h starting immediately before the onset of acoustic overexposure. The threshold shift of the auditory brainstem response (ABR) and hair cell loss were then evaluated one and two weeks after acoustic overexposure. Tempol and 3-aminobenzamide significantly protected the cochlea against acoustic injury, whereas the NOS inhibitors did not exert any protective effect. These findings suggest that reactive oxygen species and PARS are involved in acoustic injury of the cochlea. However, further study is necessary to elucidate the roles of nitric oxide and nitric oxide synthase in acoustic injury.

Analysis of Variance↗

PubMed2006

Protective effects of glucocorticoids on ischemia-reperfusion injury of outer hair cells.

OBJECTIVE: This animal study aimed to investigate effects of glucocorticoids on the functional recovery of outer hair cells (OHCs) after transient ischemia. METHODS: Distortion-product otoacoustic emission (DPOAE) was examined before, during, and after transient cochlear ischemia of 30 minutes using albino guinea pigs. RESULTS: DPOAE decreased to noise level during ischemia. On recirculation, DPOAE initially recovered with time until 20 minutes after the onset of reperfusion, but thereafter, the DPOAE level gradually decreased toward the noise level in the control animals. Prednisolone and methylprednisolone significantly improved the DPOAE level 60 minutes after the onset of reperfusion. CONCLUSIONS: The present findings suggest that glucocorticoids possess protective effects against ischemia-reperfusion injury of OHCs.

Animals↗

PubMed2005

Dehydroepiandrosterone sulfate reduces acoustic injury of the guinea-pig cochlea.

The present study was performed to determine effects of dehydroepiandrosterone sulfate (DHEAS), a neurosteroid, on acoustic injury. Albino guinea pigs were exposed to a 2 kHz pure tone of 120 or 125 dB sound pressure level for 10 min immediately after intravenous administration of DHEAS. Statistically significant improvement in the compound action potential threshold shifts and in amplitude reduction of distortion-product otoacoustic emissions was observed 1 week after the acoustic overexposure in the animals treated with DHEAS. The present results suggest that DHEAS has a protective effect against acoustic injury of the cochlea.

Acoustic Stimulation↗

PubMed2005

Coexistence of pemphigus vulgaris and bullous pemphigoid in the upper aerodigestive tract.

Pemphigus vulgaris and bullous pemphigoid are autoimmune blistering diseases of the skin and the mucosa characterized by circulating autoantibodies. Coexistence of these lesions is extremely uncommon. We report herein a case of both pemphigus vulgaris and bullous pemphigoid which occurred in the upper aerodigestive tract. The diagnosis was made based on the circulating autoantibodies and direct immunofluorescent studies. The literature on this subject is reviewed.

Aged↗

PubMed2003

Glucocorticoids and dehydroepiandrosterone sulfate ameliorate ischemia-induced injury of the cochlea.

This study aimed to evaluate the effects of steroidal drugs on the functional recovery of the cochlea after transient ischemia. Albino guinea pigs were subjected to transient cochlear ischemia of 30 min duration, and the threshold shifts of the compound action potential (CAP) from the pre-ischemic values were evaluated 4 h after ischemia. Pre-ischemic administration of a glucocorticoid, prednisolone or methylprednisolone, significantly ameliorated the post-ischemic CAP threshold shifts as compared with control animals at a relatively wide range of doses. Post-ischemic administration of these glucocorticoids also exhibited protective effects. Pre-ischemic administration of dehydroepiandrosterone sulfate significantly decreased the post-ischemic CAP threshold shifts 4 h after ischemia. The present results indicate that glucocorticoids and dehydroepiandrosterone sulfate possess therapeutic effects against ischemic injury of the cochlea, such as idiopathic sudden sensorineural hearing loss.

Action Potentials↗

PubMed2002

Long-term observations on the reversibility of cochlear dysfunction after transient ischemia.

To examine the reversibility of functional damage to the cochlea after transient ischemia, cochlear ischemia of 0-60 min was induced in 34 albino guinea pigs. Thresholds of auditory brainstem response (ABR) were then followed for 5 days after ischemia. Although the ABR threshold returned to almost the pre-ischemic value after 15 min ischemia, ischemia of 30 and 60 min duration induced irreversible dysfunction. Aminoguanidine, an inducible NO synthase (iNOS) inhibitor, significantly ameliorated the post-ischemic cochlear dysfunction induced by 60 min ischemia. Morphological findings of the hair cells were consistent with these functional results. These results indicate that ischemia of 30 min or longer induces irreversible damage to the cochlea and that iNOS plays injury-producing roles in this type of injury.

Animals↗

PubMed2002

Outer hair cells functionally and structurally deteriorate during reperfusion.

Transient ischemia of the cochlea was induced in 65 albino guinea pigs by pressing the labyrinthine artery, and the effects of cochlear reperfusion on cochlear potentials (endocochlear potential, compound action potential and cochlear microphonics (CM)) and structural changes in hair cells were examined. Although 15 min ischemia did not elevate the post-ischemic CM pseudo-threshold as compared with the pre-ischemic value, ischemia of 30 min or longer significantly elevated the CM pseudo-threshold. CM amplitude tended to progressively decrease during the reperfusion period in the animals subjected to 45 or 60 min ischemia. After transient ischemia, outer hair cells (OHCs) were swollen and exhibited alterations of the nucleus. Severer structural deterioration of OHCs was induced by 4 h reperfusion than ischemia itself when the ischemic period was 45 or 60 min. Perilymphatic perfusion of dimethylthiourea, a hydroxyl radical scavenger, partially ameliorated the elevation of the CM pseudo-thresholds and the structural changes of OHCs. These results indicate that cochlear reperfusion induces functional and structural deterioration of OHC probably by hydroxyl radical generation.

Action Potentials↗

PubMed2002

Effect of ketamine, dextromethorphan, and MK-801 on cochlear dysfunction induced by transient ischemia.

Overstimulation of the N-methyl-D-aspartate (NMDA) glutamate receptor has been implicated as a factor in the pathogenesis of hypoxic-ischemic injury in the central nervous system. To evaluate the role played by NMDA antagonists in ischemia-reperfusion injury of the cochlea, 3 noncompetitive NMDA antagonists--ketamine, dextromethorphan, and MK-801--were administered to 53 albino guinea pigs subjected to transient ischemia of 30 minutes' duration, and the threshold shifts of the compound action potential were compared with those of nontreated animals 4 hours after the onset of recirculation. Ketamine and dextromethorphan moderately ameliorated the compound action potential threshold shifts, whereas MK-801, the most potent NMDA receptor antagonist among these 3 agents, did not show any protective effect. These results indicate that the action antagonizing the NMDA receptor has no protective effect against ischemia-reperfusion injury of the cochlea, and that ketamine and dextromethorphan act as protective agents for the cochlea via other pathways.

Action Potentials↗

PubMed2002

Does endogenous or exogenous adenosine facilitate the functional recovery of the cochlea after ischemia?

The present study was undertaken to determine whether adenosine attenuates cochlear dysfunction induced by transient ischemia. Adenosine or erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA), an adenosine deaminase inhibitor, was administered by perilymphatic perfusion to albino guinea pigs that were subjected to cochlear ischemic episodes of 30-minute duration. The threshold shift of the compound action potential (CAP) from the preischemic value was significantly reduced in the animals perfused with EHNA 1 hour after the onset of reperfusion. However, perfusion of adenosine at concentrations of 100 micromol/L to 10 mmol/L did not reduce the postischemic CAP threshold shift by either 1 hour or 4 hours after the onset of reperfusion. These results suggest that the elevation of the adenosine concentration did not exert a protective effect on the cochlear ischemia-reperfusion injury, and that the protective action of EHNA is unrelated to elevating the adenosine concentration.

Action Potentials↗