thromboxane-a2 and Hearing-Loss--Sensorineural

thromboxane-a2 has been researched along with Hearing-Loss--Sensorineural* in 2 studies

Other Studies

2 other study(ies) available for thromboxane-a2 and Hearing-Loss--Sensorineural

ArticleYear
Possible role of HMG-CoA reductase inhibitors for the treatment of sudden sensorineural hearing loss (SSHL).
    Medical hypotheses, 2002, Volume: 58, Issue:5

    The term 'idiopathic' is used to design sudden sensorineural hearing loss when causative factors cannot be identified. In most cases a viral infection or a circulatory defect are considered to play a significant role when an alternative satisfactory explanation cannot be found. However some significant points remain unclear, since the great variability in age and general conditions of the affected people makes it difficult to find a reliable interpretation of the exact nature of this phenomenon which is reasonably considered to have a multifactorial origin. Under these conditions many different therapeutic strategies have been put forward, thus suggesting some degree of uncertainty not only about the pathogenetic mechanisms of the disease but also on the actual effectiveness of the disparate treatment approaches. In this paper the use of statins in sudden sensorineural hearing loss is firstly proposed on the basis of their metabolic and hemodynamic effects, and the possible clinical implications are outlined.

    Topics: Cochlea; Hearing Loss, Sensorineural; Hearing Loss, Sudden; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Models, Biological; Receptor, Angiotensin, Type 1; Receptors, Angiotensin; Thromboxane A2

2002
Altered effect of arachidonic acid on inner ear blood flow in rats with streptozotocin-induced diabetes.
    The Annals of otology, rhinology, and laryngology, 1991, Volume: 100, Issue:5 Pt 1

    The present study was undertaken to clarify the altered effect of arachidonic acid on inner ear blood flow in rats with streptozotocin-induced diabetes by use of the laser-Doppler flowmeter. Drugs were administered intraarterially via the subclavian artery in a dose range that did not affect the systemic blood pressure. Both arachidonic acid and papaverine hydrochloride increased inner ear blood flow dose-dependently. Diabetic rats at 12 weeks, but not at 8 weeks, after the induction of diabetes showed a significant decrease in arachidonic acid response. However, there were no differences in papaverine response between diabetic and control rats. Pretreatment with ONO-3708, a selective thromboxane A2 antagonist, reversed the attenuated response to arachidonic acid found in diabetic rats. An increased response to thromboxane A2, which decreased inner ear blood flow, was also found in 12-week diabetic rats. In electrocochleograms, the latency in 12-week diabetic rats was significantly delayed compared with that in control rats, and this prolonged latency improved with insulin treatment. These results suggest that the responsiveness of inner ear blood flow to prostaglandins may be altered in individuals with diabetes mellitus.

    Topics: Animals; Arachidonic Acid; Arachidonic Acids; Audiometry, Evoked Response; Diabetes Mellitus, Experimental; Diabetic Angiopathies; Ear, Inner; Hearing Loss, Sensorineural; Male; Papaverine; Rats; Rats, Inbred Strains; Regional Blood Flow; Stimulation, Chemical; Thromboxane A2; Time Factors

1991