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  • Cardioprotection with adenosine metabolism inhibitors in ischemic-reperfused mouse heart

    Author(s)
    Peart, J
    Matherne, GP
    Cerniway, RJ
    Headrick, JP
    Griffith University Author(s)
    Headrick, John P.
    Peart, Jason N.
    Year published
    2001
    Metadata
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    Abstract
    Objectives: To characterize the 'anti-ischemic' effects of adenosine metabolism inhibition in ischemic-reperfused myocardium. Methods: Perfused C57/B16 mouse hearts were subjected to 20 min ischemia 40 min reperfusion in the absence or presence of adenosine deaminase inhibition (50 占erythro-2-(2-hydroxy-3-nonyl)adenine; EHNA) adenosine kinase inhibition (10 占iodotubercidin; IODO), or 10 占adenosine. Hearts overexpressing A1 adenosine receptors (A1ARs) were also studied. Results: EHNA treatment reduced ischemic contracture and post-ischemic diastolic pressure (14Რvs. 20ᱠmmHg), increased recovery of developed pressure (66᳠vs. ...
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    Objectives: To characterize the 'anti-ischemic' effects of adenosine metabolism inhibition in ischemic-reperfused myocardium. Methods: Perfused C57/B16 mouse hearts were subjected to 20 min ischemia 40 min reperfusion in the absence or presence of adenosine deaminase inhibition (50 占erythro-2-(2-hydroxy-3-nonyl)adenine; EHNA) adenosine kinase inhibition (10 占iodotubercidin; IODO), or 10 占adenosine. Hearts overexpressing A1 adenosine receptors (A1ARs) were also studied. Results: EHNA treatment reduced ischemic contracture and post-ischemic diastolic pressure (14Რvs. 20ᱠmmHg), increased recovery of developed pressure (66᳠vs. 53Ქ) and reduced LDH efflux (8.9ᱮ6 vs. 18.0ᱮ7 I.U./g). IODO also improved functional recovery (to 60Ქ) and reduced LDH efflux (5.3ᱮ7 I.U./g), as did treatment with 10 占adenosine. Protection with EHNA was reversed by co-infusion of IODO or 50 占8-?-sulfophenyltheophylline (adenosine receptor antagonist), but unaltered by 20 占inosine+10 孠hypoxanthine. Similarly, effects of iodotubercidin were inhibited by EHNA and 8-?-sulfophenyltheophylline. A1AR overexpression exerted similar effects to EHNA and EHNA or IODO alone enhanced recovery while EHNA+IODO reduced recovery in transgenic hearts. Functional recoveries and xanthine oxidase reactant levels were unrelated in the groups studied. Conclusions: Adenosine deaminase or kinase inhibition protects from ischemia-reperfusion. Cardioprotection via these enzyme inhibitors requires a functioning purine salvage pathway and involves enhanced adenosine receptor activation. Reduced formation of inosine is unimportant in EHNA-mediated protection.
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    Journal Title
    Cardiovascular Research
    Volume
    52
    Publisher URI
    https://academic.oup.com/cardiovascres/article/52/1/120/295362
    Copyright Statement
    © 2001 Elsevier : Reproduced in accordance with the copyright policy of the publisher : This journal is available online - use hypertext links.
    Subject
    Cardiovascular medicine and haematology
    Publication URI
    http://hdl.handle.net/10072/3752
    Collection
    • Journal articles

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