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This dissertation, Intermittent Hypoxia Mediates Cardioprotection via Calcium Handling Mechanisms by Hang-mee, Yeung, 楊恆美, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled 'Intermittent Hypoxia Mediates Cardioprotection via Calcium Handling Mechanisms' submitted by Yeung Hang Mee for the Degree of Master of Philosophy at the University of Hong Kong in August, 2006. 2+ This study investigated calcium (Ca ) handling mechanisms involved in cardioprotection induced by intermittent hypoxia (IH) against ischemia-reperfusion (I/R) injury. Adult male Sprague-Dawley rats were exposed to 10% inspired O continuously for 6 hours daily from 3 to 14 days. In isolated perfused hearts subjected to I/R, IH-induced cardioprotection was most significant in the 7-day group with less infarct size and lactate dehydrogenase release comparing with normoxic group. The amplitude, decay time and time to peak of both electrically- 2+ and caffeine-induced Ca transients measured by spectrofluorometry in isolated ventricular myocytes of 7-day IH group were less deteriorated in I/R than that of the 2+ normoxic group, suggesting an improved Ca handling of the sarcoplasmic reticulum (SR) and sarcolemma. 45 2+ We further determined the protein expression and activity of Ca flux of SR- 2+ + 2+ Ca -ATPase (SERCA), ryanodine receptor (RyR) and sarcolemmal Na /Ca exchange (NCX) in ventricular myocytes from the IH and normoxic groups before ii2+ and during MI/A-R. There were no changes in expression levels of the Ca -handling proteins but significant increases in the RyR and NCX activities were remarkable during MI/A-R in the IH but not the normoxic group. The augmented RyR and NCX activities were abolished respectively by PKA inhibitor KT5720 (0.5 μM) and PKC 2+ inhibitor chelerythrine chloride (5 μM) but not by Ca /calmodulin-dependent protein kinase II inhibitor KN-93 (1μM). To conclude, IH confers cardioprotection 2+ against I/R injury in rat cardiomyocytes by ameliorated Ca handling with augmented RyR and NCX activities via protein kinases activation. iii DOI: 10.5353/th_b3750105 Subjects: AnoxemiaCalciumReperfusion injuryIschemiaHeart - Physiology

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