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  • Pre- or post-ischemic bilirubin ditaurate treatment reduces oxidative tissue damage and improves cardiac function

    Author(s)
    Bakrania, Bhavisha
    Du Toit, Eugene F
    Wagner, Karl-Heinz
    Headrick, John P
    Bulmer, Andrew C
    Griffith University Author(s)
    Headrick, John P.
    Bakrania, Bhavisha
    Du Toit, Eugene
    Bulmer, Andrew C.
    Wagner, Karl-Heinz
    Year published
    2016
    Metadata
    Show full item record
    Abstract
    Background Unconjugated bilirubin (UCB), an endogenous antioxidant, may protect the heart against ischemia–reperfusion (I–R) injury. However, the ‘cardioprotective’ potential of bilirubin therapy remains unclear. We tested whether pre- or post-ischemic treatment of ex vivo perfused hearts with bilirubin ditaurate (BRT) improves post-ischemic functional outcomes and myocardial oxidative damage. Methods Isolated Langendorff perfused hearts (male, Wistar rats) were treated with 50 μM BRT for 30 min before (Pre) or after (Post) 30 min of zero-flow ischemia. Functional outcomes were monitored, with myocardial damage estimated ...
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    Background Unconjugated bilirubin (UCB), an endogenous antioxidant, may protect the heart against ischemia–reperfusion (I–R) injury. However, the ‘cardioprotective’ potential of bilirubin therapy remains unclear. We tested whether pre- or post-ischemic treatment of ex vivo perfused hearts with bilirubin ditaurate (BRT) improves post-ischemic functional outcomes and myocardial oxidative damage. Methods Isolated Langendorff perfused hearts (male, Wistar rats) were treated with 50 μM BRT for 30 min before (Pre) or after (Post) 30 min of zero-flow ischemia. Functional outcomes were monitored, with myocardial damage estimated from creatine kinase efflux, infarct size, and left ventricular lipid/protein oxidation assessed by measuring malondialdehyde and protein carbonyls. Ischemia induced contractile dysfunction and cellular injury, with both BRT treatments improving I–R outcomes. Results Final post-ischemic recoveries for left ventricular diastolic/developed pressures were significantly enhanced in treated groups: end-diastolic pressure (Control, 78 ± 14, Pre, 51 ± 15*, Post, 51 ± 13 mm Hg*); left ventricular developed pressure, (LVDP; Control 44 ± 15, Pre, 71 ± 19*, Post, 84 ± 13 mm Hg*). Myocardial injury/infarction (MI) was also significantly reduced with BRT treatment: post-ischemic creatine kinase efflux (Control, 1.24 ± 0.41, Pre, 0.86 ± 0.31*, Post, 0.51 ± 0.29 U/g/mL*; infarct size, Control, 67 ± 17, Pre, 39 ± 15*, Post, 22 ± 11%*). These changes were accompanied by significantly reduced malondialdehyde and protein carbonyl content in Pre and Post treated hearts (*P < 0.05 vs. Control). Conclusions These data collectively reveal significant cardioprotection upon BRT treatment, with post-treatment being particularly effective. Significant reductions in infarct size and lipid and protein oxidation indicate a mechanism related to protection from oxidative damage and indicate the potential utility of this molecule as a post-MI treatment.
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    Journal Title
    International Journal of Cardiology
    Volume
    202
    DOI
    https://doi.org/10.1016/j.ijcard.2015.08.192
    Subject
    Cardiology (incl. Cardiovascular Diseases)
    Cardiorespiratory Medicine and Haematology
    Public Health and Health Services
    Publication URI
    http://hdl.handle.net/10072/99447
    Collection
    • Journal articles

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