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ototoxicity/kalium
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Seite 1 von 39 Ergebnisse
Potassium ion channel openers, Maxipost and Retigabine, protect against peripheral salicylate ototoxicity in rats.
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Sodium Salicylate (SS) reliably induces a sensorineural hearing loss and tinnitus when administered in high doses. Recent animal modeled studies indicate that potassium channel openers such as Maxipost and Retigabine (RTG) can block SS- or noise-induced tinnitus respectively; however, the origins
[Clinical and experimental studies on ototoxicity of potassium bromate].
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Effect of low-dose prophylactic dopamine on high-dose cisplatin-induced electrolyte wasting, ototoxicity, and epidermal growth factor excretion: a randomized, placebo-controlled, double-blind trial.
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OBJECTIVE
To evaluate the protective effect of low-dose dopamine given as continuous infusion in patients who undergo chemotherapy with the nephrotoxin cisplatin.
METHODS
Forty-two patients who received high-dose cisplatin-containing chemotherapy entered a prospective, randomized, double-blind,
Bromate-induced ototoxicity.
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For decades, it has been known that ingested potassium bromate and sodium bromate can induce hearing loss. Hearing loss onset, following high-dose ingestion, is generally rapid occurring within 4-16 h and of a severe to profound degree. Unlike the sensorineural hearing loss which is generally
Continuous or repeated prolonged cisplatin infusions in children: a prospective study on ototoxicity, platinum concentrations, and standard serum parameters.
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BACKGROUND
To overcome the ototoxicity of cisplatin, single bolus infusions were replaced by repeated prolonged infusions of lower doses or by continuous infusions at still lower infusion rates. However, considering ototoxicity little is, in fact, known about the tolerance of repeated prolonged or
Computational model of vectorial potassium transport by cochlear marginal cells and vestibular dark cells.
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Cochlear marginal cells and vestibular dark cells transport potassium into the inner ear endolymph, a potassium-rich fluid, the homeostasis of which is essential for hearing and balance. We have formulated an integrated mathematical model of ion transport across these epithelia that incorporates the
Acute cochleovestibular toxicity due to topical application of potassium iodide.
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We present a case report of a patient who suffered from an acute cochleovestibular deficit after topical application of potassium iodide solution into the left ear. Although the vestibular symptoms progressively disappeared, severe sensorineural hearing loss persisted after treatment with hyperbaric
Mercury (Hg2+) suppression of potassium currents of outer hair cells.
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The heavy metal mercury (Hg(2+)) is an insidious environmental pollutant that causes toxic effects on sensory systems. It is well known that the group IIB divalent cation Hg(2+) is an inhibitor of the group I monovalent potassium (K(+)) cation pore-forming channel in several biological preparations.
Round window membrane permeability during experimental purulent otitis media: altered Cortisporin ototoxicity.
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Round window membrane (RWM) permeability is the most critical factor influencing cochlear function following otitis media. Because otic drops are frequently used during purulent otitis media (POM), we investigated RWM permeability and ototoxicity of Cortisporin otic suspension after inducing
The effects of cetrimide and potassium bromate on the potassium ion concentration in the inner ear fluid of the guinea-pig.
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The mammalian inner ear is located deep within the temporal bone. The organ of Corti, the delicate sensory system for sound, is surrounded by two fluid systems; the potassium-rich endolymph and the sodium-rich perilymph. The pathogenesis of inner ear deafness is thought to be largely due to an
Effect of glucarolactam on ototoxicity of aminoglycoside antibiotics in guinea-pigs.
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Intramuscular administration of glucarolactam in the form of aminoglycoside salt to guinea-pigs protected the experimental ototoxicity caused by high dosing of aminoglycoside antibiotics. The protection was evidenced by the pinna reflex threshold and histochemical examinations of hair cells of
Ototoxicity of salicylate, nonsteroidal antiinflammatory drugs, and quinine.
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Salicylates and most NSAIDS in high doses cause mild to moderate temporary hearing loss, either flat or greater in the high frequencies. Hearing loss is accompanied by tinnitus and suprathreshold changes. Salicylates may or may not exacerbate hearing loss and cochlear damage induced by noise. The
Inhibition of the calcium- and voltage-dependent big conductance potassium channel ameliorates cisplatin-induced apoptosis in spiral ligament fibrocytes of the cochlea.
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The role of calcium- and voltage-dependent big conductance potassium channels in regulating apoptosis was investigated in cultured type I spiral ligament fibrocytes. Incubation of type I spiral ligament fibrocytes derived from gerbil cochlea with cisplatin induced dose- and time-dependent apoptosis
Ototoxicity of topical ticarcillin and clavulanic acid in the chinchilla.
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BACKGROUND
Currently available topical otic preparations contain a variety of antibiotics and other ingredients that are potentially damaging to the middle and inner ear. There is therefore a need to identify agents that are safe as well as effective for topical otologic use. In pursuit of that
Bumetanide hyperpolarizes madin-darby canine kidney cells and enhances cellular gentamicin uptake by elevating cytosolic Ca(2+) thus facilitating intermediate conductance Ca(2+)--activated potassium channels.
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Loop diuretics such as bumetanide and furosemide enhance aminoglycoside ototoxicity when co-administered to patients and animal models. The underlying mechanism(s) is poorly understood. We investigated the effect of these diuretics on cellular uptake of aminoglycosides, using Texas Red-tagged
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