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Conference Paper: Chronic intermittent hypoxia exacerbates oxidative stress and deteriorates calcium homeostasis in rat hearts

TitleChronic intermittent hypoxia exacerbates oxidative stress and deteriorates calcium homeostasis in rat hearts
Authors
Yeung, PHMHung, MWKravtsov, GMFung, ML
Issue Date2009
PublisherAmerican Heart Association (AHA).
Citation
The 63rd Annual High Blood Pressure Research Conference, Chicago, IL., 23-26 September 2009. How to Cite?
AbstractOBJECTIVES: In our study we hypothesized that chronic intermittent hypoxia mimicking obstructive sleep apnea aggravates oxidative stress and impairs calcium (Ca2+) -handling in rat cardiac myocytes. METHODS: Adult male 2-month old Sprague-Dawley rats were daily administered with melatonin (MIH, 10mg/Kg/day of body weight, i.p.) or vehicle (VIH, 2% ethanol in normal saline) and exposed to intermittent hypoxic chamber (inspired oxygen alternating from 21 to 5 +/- 0.5% oxygen per minute for 8 hr/day) for 28 days. Levels of malodialdehyde (MDA) and the mRNA expressions of anti-oxidant enzymes in all rat hearts were determined by colorimetric study and reverse transcription-PCR respectively. Impairments of sarcoplasmic reticulum (SR) Ca2+ -handling were measured by spectrofluorometer in isolated fura-2-loaded ventricular myocytes from all rat groups. And the differences in protein expressions and activities of SR - Ca2+ handling proteins were measured by western blot and 45Ca2+ flux study in the ventricular myocytes from all rat groups. RESULTS: The ratio of heart weight to body weight and the production of MDA were significantly more in VIH group than that of normoxic and MIH groups. In addition, the mRNA levels of catalase and Mn-superoxide dismutase in VIH group were much less than that of other two groups. Moreover, spectroflurometric studies showed that decreases in SR - Ca2+ content and the metabolic inhibition/anoxia induced intracellular Ca2+ overload were much remarkable in VIH ventricular myocytes compared to the normoxic control. Also the protein levels and activities of SR Ca2+ -ATPase and sarcolemmal Na+ - Ca2+ exchanger were markedly reduced in VIH cardiomyocytes. However, those impairments were significantly ameliorated in MIH group. CONCLUSIONS: In this study we show that chronic intermittent hypoxia leading to myocardial injuries by severe oxidative stress and impairments of SR Ca2+ handling in rat cardiomyocytes.
DescriptionPoster Presentations: P113
Persistent Identifierhttp://hdl.handle.net/10722/126738

 

DC FieldValueLanguage
dc.contributor.authorYeung, PHMen_HK
dc.contributor.authorHung, MWen_HK
dc.contributor.authorKravtsov, GMen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-10-31T12:45:41Z-
dc.date.available2010-10-31T12:45:41Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 63rd Annual High Blood Pressure Research Conference, Chicago, IL., 23-26 September 2009.en_HK
dc.identifier.urihttp://hdl.handle.net/10722/126738-
dc.descriptionPoster Presentations: P113-
dc.description.abstractOBJECTIVES: In our study we hypothesized that chronic intermittent hypoxia mimicking obstructive sleep apnea aggravates oxidative stress and impairs calcium (Ca2+) -handling in rat cardiac myocytes. METHODS: Adult male 2-month old Sprague-Dawley rats were daily administered with melatonin (MIH, 10mg/Kg/day of body weight, i.p.) or vehicle (VIH, 2% ethanol in normal saline) and exposed to intermittent hypoxic chamber (inspired oxygen alternating from 21 to 5 +/- 0.5% oxygen per minute for 8 hr/day) for 28 days. Levels of malodialdehyde (MDA) and the mRNA expressions of anti-oxidant enzymes in all rat hearts were determined by colorimetric study and reverse transcription-PCR respectively. Impairments of sarcoplasmic reticulum (SR) Ca2+ -handling were measured by spectrofluorometer in isolated fura-2-loaded ventricular myocytes from all rat groups. And the differences in protein expressions and activities of SR - Ca2+ handling proteins were measured by western blot and 45Ca2+ flux study in the ventricular myocytes from all rat groups. RESULTS: The ratio of heart weight to body weight and the production of MDA were significantly more in VIH group than that of normoxic and MIH groups. In addition, the mRNA levels of catalase and Mn-superoxide dismutase in VIH group were much less than that of other two groups. Moreover, spectroflurometric studies showed that decreases in SR - Ca2+ content and the metabolic inhibition/anoxia induced intracellular Ca2+ overload were much remarkable in VIH ventricular myocytes compared to the normoxic control. Also the protein levels and activities of SR Ca2+ -ATPase and sarcolemmal Na+ - Ca2+ exchanger were markedly reduced in VIH cardiomyocytes. However, those impairments were significantly ameliorated in MIH group. CONCLUSIONS: In this study we show that chronic intermittent hypoxia leading to myocardial injuries by severe oxidative stress and impairments of SR Ca2+ handling in rat cardiomyocytes.-
dc.languageengen_HK
dc.publisherAmerican Heart Association (AHA).-
dc.relation.ispartofAnnual High Blood Pressure Research Conference-
dc.rightsThis is an un-copyedited author manuscript that was accepted for publication in (journal name), © The American Heart Association. This may not be duplicated or reproduced, other than for personal use or within the ‘Fair Use of Copyrighted Materials’ (section 107, title 17, U.S. Code) without prior permission of the copyright owner, The American Heart Association. The final copyedited article, which is the version of record, can be found at (journal URL). The American Heart Association disclaims any responsibility or liability for errors or omissions in this version of the manuscript or in any version derived from it by the National Institutes of Health or other parties.-
dc.titleChronic intermittent hypoxia exacerbates oxidative stress and deteriorates calcium homeostasis in rat heartsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailYeung, PHM: hangmee@gmail.comen_HK
dc.identifier.emailHung, MW: philiphung928@hotmail.comen_HK
dc.identifier.emailKravtsov, GM: gmkravts@HKUCC.hku.hk-
dc.identifier.emailFung, ML: fungml@hkucc.hku.hk-
dc.identifier.hkuros179013en_HK

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