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Endolymphatic perfusion with EGTA-acetoxymethyl ester inhibits asphyxia- and furosemide-induced decrease in endocochlear potential in guinea pigs.
Jpn J Physiol. 2005 Feb; 55(1):53-60.JJ

Abstract

We examined the effect of the Ca(2+) concentration in the endolymph ([Ca](e)) or in the endolymphatic surface cells ([Ca](i)) on the endocochlear potential (EP) by using an endolymphatic or perilymphatic perfusion technique, respectively. (i) A large increase in [Ca](e) up to approximately 10(-3) M with a fall in the EP was induced by transient asphyxia (approximately 2 min) or by the intravenous administration of furosemide (60 mg/kg), and a significant correlation was obtained between the EP and p[Ca](e) (= -log [Ca](e), r = 0.998). (ii) Perfusion of the endolymph with 10 mM EGTA for 5 min neither produced any significant change in the EP nor altered the asphyxia-induced change in EP (DeltaEP(asp)), suggesting that neither [Ca](e) nor the Ca(2+) concentration gradient across the stria vascularis contributed directly to the generation of the EP in the condition of low [Ca](e). In contrast, endolymphatic perfusion with high Ca(2+) (more than 10 mM) produced a decrease in EP and a significant correlation was obtained between the EP and the Ca(2+) concentration of perfusion solution (r = 0.982), suggesting that Ca(2+) permeability may exist across the stria vascularis. (iii) The administration of a Ca(2+) chelator, EGTA-acetoxymethyl ester (AM, 0.3 mM), to the endolymph, which produced a gradual increase in EP, suppressed significantly, by 60-80%, DeltaEP(asp) or furosemide-induced changes in EP. In contrast, perilymphatic administration of 0.5 mM EGTA-AM caused no significant suppression of the DeltaEP(asp). These findings suggest that [Ca](i) plays an important role in generating/maintaining a large positive EP.

Authors+Show Affiliations

Department of Physiology II and Department of Otolaryngology, Osaka Medical College, Takatsuki, Osaka, 569-8686 Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15796789

Citation

Mineharu, Akihito, et al. "Endolymphatic Perfusion With EGTA-acetoxymethyl Ester Inhibits Asphyxia- and Furosemide-induced Decrease in Endocochlear Potential in Guinea Pigs." The Japanese Journal of Physiology, vol. 55, no. 1, 2005, pp. 53-60.
Mineharu A, Mori Y, Nimura Y, et al. Endolymphatic perfusion with EGTA-acetoxymethyl ester inhibits asphyxia- and furosemide-induced decrease in endocochlear potential in guinea pigs. Jpn J Physiol. 2005;55(1):53-60.
Mineharu, A., Mori, Y., Nimura, Y., Takamaki, A., Araki, M., Yamaji, J., Yoshida, R., Takenaka, H., & Kubota, T. (2005). Endolymphatic perfusion with EGTA-acetoxymethyl ester inhibits asphyxia- and furosemide-induced decrease in endocochlear potential in guinea pigs. The Japanese Journal of Physiology, 55(1), 53-60.
Mineharu A, et al. Endolymphatic Perfusion With EGTA-acetoxymethyl Ester Inhibits Asphyxia- and Furosemide-induced Decrease in Endocochlear Potential in Guinea Pigs. Jpn J Physiol. 2005;55(1):53-60. PubMed PMID: 15796789.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endolymphatic perfusion with EGTA-acetoxymethyl ester inhibits asphyxia- and furosemide-induced decrease in endocochlear potential in guinea pigs. AU - Mineharu,Akihito, AU - Mori,Yoshiaki, AU - Nimura,Yoshitsugu, AU - Takamaki,Atsuko, AU - Araki,Michitoshi, AU - Yamaji,Junko, AU - Yoshida,Ryotaro, AU - Takenaka,Hiroshi, AU - Kubota,Takahiro, PY - 2005/3/31/pubmed PY - 2005/8/10/medline PY - 2005/3/31/entrez SP - 53 EP - 60 JF - The Japanese journal of physiology JO - Jpn J Physiol VL - 55 IS - 1 N2 - We examined the effect of the Ca(2+) concentration in the endolymph ([Ca](e)) or in the endolymphatic surface cells ([Ca](i)) on the endocochlear potential (EP) by using an endolymphatic or perilymphatic perfusion technique, respectively. (i) A large increase in [Ca](e) up to approximately 10(-3) M with a fall in the EP was induced by transient asphyxia (approximately 2 min) or by the intravenous administration of furosemide (60 mg/kg), and a significant correlation was obtained between the EP and p[Ca](e) (= -log [Ca](e), r = 0.998). (ii) Perfusion of the endolymph with 10 mM EGTA for 5 min neither produced any significant change in the EP nor altered the asphyxia-induced change in EP (DeltaEP(asp)), suggesting that neither [Ca](e) nor the Ca(2+) concentration gradient across the stria vascularis contributed directly to the generation of the EP in the condition of low [Ca](e). In contrast, endolymphatic perfusion with high Ca(2+) (more than 10 mM) produced a decrease in EP and a significant correlation was obtained between the EP and the Ca(2+) concentration of perfusion solution (r = 0.982), suggesting that Ca(2+) permeability may exist across the stria vascularis. (iii) The administration of a Ca(2+) chelator, EGTA-acetoxymethyl ester (AM, 0.3 mM), to the endolymph, which produced a gradual increase in EP, suppressed significantly, by 60-80%, DeltaEP(asp) or furosemide-induced changes in EP. In contrast, perilymphatic administration of 0.5 mM EGTA-AM caused no significant suppression of the DeltaEP(asp). These findings suggest that [Ca](i) plays an important role in generating/maintaining a large positive EP. SN - 0021-521X UR - https://www.unboundmedicine.com/medline/citation/15796789/Endolymphatic_perfusion_with_EGTA_acetoxymethyl_ester_inhibits_asphyxia__and_furosemide_induced_decrease_in_endocochlear_potential_in_guinea_pigs_ L2 - http://joi.jlc.jst.go.jp/JST.JSTAGE/jjphysiol/R2086?from=PubMed DB - PRIME DP - Unbound Medicine ER -