Experiments on Temporary Obstruction of the Internal Auditory Artery.

Perlman, H. B.; Kimura, Atsushi; Fernández, Ceneida

doi:10.1288/00005537-195906000-00001

Cited by 304 publications

(104 citation statements)

References 18 publications

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“…24,25 The administration of GM in 125 mg/kg alone could not produce prolonged significant ABR threshold shifts or HC loss, consistent with previous study. 29 However, administration of GM after transient cochlear ischemia elicited significant auditory threshold shifts (Figure 1).…”

Section: Discussionsupporting

confidence: 89%

“…Ventral approach to labyrinthine artery has been described. 24,25 In brief, electrodes were inserted subcutaneously into the left mastoid (anode), right mastoid (cathode), and back (ground) and an earphone inserted into the left ear canal to monitor auditory brainstem responses (ABRs) perioperatively. A submental incision was made medially to mandibular edge.…”

Section: Materials and Methods Transient Cochlear Ischemia Modelmentioning

confidence: 99%

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Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Kao

Tsai

Lai

et al. 2011

Laboratory Investigation

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Aminoglycoside ototoxicity is a common cause of drug-induced hearing loss. Toxicity is dose related, but some patients may still develop hearing loss even under safe dosage. Apart for genetic idiosyncrasy, indirect evidences imply that ischemia may increase the aminoglycoside ototoxic sensitivity because common clinical situations associated with cochlear ischemia such as noise, sepsis, and shock are known to augment the development of aminoglycoside ototoxicity. At present, a direct interaction of cochlear ischemia and aminoglycoside ototoxicity is still lacking. This study demonstrated a direct evidence of increased gentamicin (GM) ototoxic sensitivity in chronic guinea pig models of transient cochlear ischemia. No permanent auditory changes were observed after a single dose of GM (125 mg/kg) or after transient cochlear ischemia for 30 min. Persistent and significant auditory threshold shift was detected when GM was given after transient cochlear ischemia. Cochlear hair cells and spiral ganglion neurons are the major regions affected. Apoptosis contributes to hair cell death during acute interaction of ischemia and GM ototoxicity. Increased apoptotic cell death was also depicted when GM crossreacted with hypoxia in vitro, using cochlear cell lines. Generation of reactive oxygen species, loss of mitochondrial membrane potential, calcium release, and caspase-dependent apoptotic cell death were shown during the interaction of hypoxia and GM ototoxicity in vitro. This synergistic ototoxicity may be critical to aminoglycoside-induced hearing loss in clinical scenarios. The results should improve our understanding of the interacting mechanism and potential preventive strategy to aminoglycoside ototoxicity.

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Section: Discussionsupporting

confidence: 89%

Section: Materials and Methods Transient Cochlear Ischemia Modelmentioning

confidence: 99%

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Kao

Tsai

Lai

et al. 2011

Laboratory Investigation

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show abstract

“…Istnieją dowody doświadczalne, że okresowe niedokrwienie ślimaka powoduje większą jego wrażliwość na ponowne niedokrwienie, pojawiające się po przywróceniu prawidłowego krążenia. Uszkodzenia spowodowane są najprawdopodobniej przez wolne rodniki uwalniane z niedokrwionych uprzednio tkanek po ponownym ukrwieniu [72,128,157,163]. W piśmiennictwie znaleźć można liczne opisy kliniczne nagłych niedosłuchów, których przyczyną były zmiany naczyniowe.…”

Section: Zaburzenia S ł Uchu I Równowagi W Chorobach Naczyniowych unclassified

“…Perlman i wsp. [163] zamykali chirurgicznie naczynia tętnicze i żylne ślimaka u świnki morskiej, co w ciągu tygodnia powodowało rozległe zniszczenie komórek słuchowych. Suga i wsp.…”

Section: Zaburzenia S ł Uchu I Równowagi W Chorobach Naczyniowych unclassified

Stan słuchu u chorych we wczesnym okresie udaru niedokrwiennego mózgu

Przewoźny¹

2007

Otolaryngologia Polska

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“…Studies have reported the marked susceptibility of the OHC to hypovolemia and/or ischemia 3 . In order to further investigate the matter, we decided to look into distortion product otoacoustic emissions (DPOAE) during heart surgery with extracorporeal circulation (ECC) and hypothermia, an event where the risk of peripheral organ ischemia is high in spite of technological progress, as it changes the pulsating blood flow driven by the heart to a continuum produced by the machine.…”

Section: Introductionmentioning

confidence: 99%