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Conference Paper: Intermittent hypoxia improves calcium homeostasis in rat cardiomyocytes and confers cardioprotection against ischemia-reperfusion injury

TitleIntermittent hypoxia improves calcium homeostasis in rat cardiomyocytes and confers cardioprotection against ischemia-reperfusion injury
Authors
Issue Date2005
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
The ISHR Australasian Section 29th Annual Scientific Meeting, Perth, Australia, 5-8 August 2005. In Journal of Molecular and Cellular Cardiology , v. 39 n. 3, p. 576, bastract no. P18 How to Cite?
AbstractCalcium (Ca2+) handling is central to cardiac function and may be involved in the cardioprotection induced by intermittent hypoxia (IH). We hypothesized that IH ameliorates the impaired Ca2+ handling during ischemia/reperfusion (I/R). Male Sprague-Dawley rats were exposed to normobaric IH (10% oxygen, 6 hours/day, 7 days). Isolated perfused hearts from the IH and control (in room air) rats were subjected to 30 minutes ischemia and 2 hours reperfusion. The I/R injuries reflected by lactate dehydrogenase (LDH) activity and infarct size (IS) were significantly reduced in the IH group (LDH: 116.0±20.5 U/ml vs. control 273.2±29.5 U/ml, P < 0.01, n=9 per group; IS: 22.2±2.6 % of risk zone vs. control 31.4±3.1 % of risk zone, P < 0.05, n=8 per group). Spectrofluorometric measurement of cytosolic Ca2+ ([Ca2+]i ) in isolated fura-2- loaded ventricular myocytes showed a decrease in the amplitude of electrically induced [Ca2+]i transients with an elevated diastolic [Ca2+]i level during metabolic inhibition and anoxia (MI/A). The MI/A-induced changes in the amplitude of [Ca2+]i transients and diastolic [Ca2+]i level were significantly less in the IH group. Also, the IH group had greater recovery in the amplitude of [Ca2+]i transients (83.3±6.0 % vs. control 66.7±4.7 %, P < 0.05, n=8 per group) and faster decay rate (τ) of the caffeine-induced [Ca2+]i transients (2.3±0.3 second vs. control 4.5±0.4 second, P < 0.01, n=6 per group). Results suggest that IH improves the [Ca2+]i handling in the cardiomyocytes and enhances tolerance against I/R injury. (supported by research grants from the RGC and URC)
Descriptionpp. 563-579 of this journal issue entitled: ISHR Perth 2005 abstracts
Persistent Identifierhttp://hdl.handle.net/10722/105282
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522

 

DC FieldValueLanguage
dc.contributor.authorYeung, HMen_HK
dc.contributor.authorWong, TMen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-25T22:27:36Z-
dc.date.available2010-09-25T22:27:36Z-
dc.date.issued2005en_HK
dc.identifier.citationThe ISHR Australasian Section 29th Annual Scientific Meeting, Perth, Australia, 5-8 August 2005. In Journal of Molecular and Cellular Cardiology , v. 39 n. 3, p. 576, bastract no. P18en_HK
dc.identifier.issn0022-2828en_HK
dc.identifier.urihttp://hdl.handle.net/10722/105282-
dc.descriptionpp. 563-579 of this journal issue entitled: ISHR Perth 2005 abstracts-
dc.description.abstractCalcium (Ca2+) handling is central to cardiac function and may be involved in the cardioprotection induced by intermittent hypoxia (IH). We hypothesized that IH ameliorates the impaired Ca2+ handling during ischemia/reperfusion (I/R). Male Sprague-Dawley rats were exposed to normobaric IH (10% oxygen, 6 hours/day, 7 days). Isolated perfused hearts from the IH and control (in room air) rats were subjected to 30 minutes ischemia and 2 hours reperfusion. The I/R injuries reflected by lactate dehydrogenase (LDH) activity and infarct size (IS) were significantly reduced in the IH group (LDH: 116.0±20.5 U/ml vs. control 273.2±29.5 U/ml, P < 0.01, n=9 per group; IS: 22.2±2.6 % of risk zone vs. control 31.4±3.1 % of risk zone, P < 0.05, n=8 per group). Spectrofluorometric measurement of cytosolic Ca2+ ([Ca2+]i ) in isolated fura-2- loaded ventricular myocytes showed a decrease in the amplitude of electrically induced [Ca2+]i transients with an elevated diastolic [Ca2+]i level during metabolic inhibition and anoxia (MI/A). The MI/A-induced changes in the amplitude of [Ca2+]i transients and diastolic [Ca2+]i level were significantly less in the IH group. Also, the IH group had greater recovery in the amplitude of [Ca2+]i transients (83.3±6.0 % vs. control 66.7±4.7 %, P < 0.05, n=8 per group) and faster decay rate (τ) of the caffeine-induced [Ca2+]i transients (2.3±0.3 second vs. control 4.5±0.4 second, P < 0.01, n=6 per group). Results suggest that IH improves the [Ca2+]i handling in the cardiomyocytes and enhances tolerance against I/R injury. (supported by research grants from the RGC and URC)-
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmccen_HK
dc.relation.ispartofJournal of Molecular and Cellular Cardiologyen_HK
dc.titleIntermittent hypoxia improves calcium homeostasis in rat cardiomyocytes and confers cardioprotection against ischemia-reperfusion injuryen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-2828&volume=39&issue=3&spage=576&epage=&date=2005&atitle=Intermittent+hypoxia+improves+calcium+homeostasis+in+rat+cardiomyocytes+and+confers+cardioprotection+against+ischemia-reperfusion+injuryen_HK
dc.identifier.emailYeung, HM: hangmee@gmail.comen_HK
dc.identifier.emailWong, TM: tm.wong@hkuspace.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.yjmcc.2005.05.010-
dc.identifier.hkuros122306en_HK
dc.identifier.volume39en_HK
dc.identifier.issue3en_HK
dc.identifier.spage576, bastract no. P18en_HK
dc.identifier.epage576, bastract no. P18-

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