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Original Article| Volume 22, ISSUE 4, P276-283, April 2013

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Pretreatment With Xenon Protected Immature Rabbit Heart From Ischaemia/Reperfusion Injury by Opening of the mitoKATP Channel

  • Qian Li
    Affiliations
    Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China
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  • Chunwei Lian
    Affiliations
    Department of Anesthesiology, The Second Affiliated Hospital of Wenzhou Medical College, Wenzhou, Zhejiang 325027, China
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  • Ronghua Zhou
    Affiliations
    Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China
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  • Tao Li
    Correspondence
    Corresponding author at: Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China. Tel.: +86 28 85423593; fax: +86 28 85423593.
    Affiliations
    Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China

    Laboratory of Anesthesiology and Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu 610041, China
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  • Xujin Xiang
    Affiliations
    Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China
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  • Bin Liu
    Correspondence
    Corresponding author. Tel.: +86 28 85423593; fax: +86 28 85423593.
    Affiliations
    Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China
    Search for articles by this author
Published:December 26, 2012DOI:https://doi.org/10.1016/j.hlc.2012.10.016

      Background

      The noble gas anaesthetic, xenon has previously been shown to protect the adult myocardium from ischaemia/reperfusion (I/R) injury, however its effect on immature myocardium is unclear. The aim of this study was to investigate the effect of xenon on the isolated immature heart.

      Methods

      Isolated, immature (2–3 weeks old) New Zealand rabbit hearts were perfused with Krebs–Henseleit buffer via Langendorff-mode. After 20 min of baseline equilibration, hearts were pretreated with 75% xenon, 75% xenon + 100 μM diazoxide, or 75% xenon + 100 μM 5-hydroxydecanoate, and then subjected to 1 h of global ischaemia and 3 h of reperfusion.

      Results

      Pretreatment with 75% xenon significantly improved cardiac function (P < 0.01 vs. the I/R group, respectively), limited myocardial infarct size (20.83 ± 2.16%, P < 0.01 vs. 35.82 ± 2.14% of the I/R group), reduced cardiac enzyme release (CK-MB, 1.00 ± 0.19 IU/L, P < 0.01 vs. 0.44 ± 0.14 IU/L of the I/R group; LDH, 6.15 ± 1.06 IU/L P < 0.01 vs. 3.49 ± 0.37 IU/L of the I/R group) and decreased apoptosis (6.17 ± 0.56%, P < 0.01 vs. 11.31 ± 0.93% of the I/R group). In addition, the mitochondrial structure changes caused by I/R injury were largely prevented by 75% xenon pretreatment (1.37 ± 0.16, P < 0.01 vs. 2.32 ± 0.13 of the I/R group). The mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channel opener diazoxide did not influence the effect of xenon, but the specific mitoKATP channel blocker 5-hydroxydecanoate completely abolished this effect.

      Conclusions

      Our study demonstrated that pretreatment with 75% xenon protected immature heart from I/R injury, and this protection was probably mediated by preservation of myocardial mitochondria and opening of mitoKATP channel.

      Keywords

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