Cardioprotective Effect of a Hemoglobin-Based Oxygen Carrier on Cold Ischemia/Reperfusion Injury

Objectives: The etiology of myocardial ischemia/reperfusion (I/R) injury is multifactorial, but activation of the innate immune system and the resulting inflammatory response are important components of I/R injury. The aim of this study was to investigate the protective effect of a hemoglobin-based...

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Bibliographic Details
Published inCardiology Vol. 120; no. 2; pp. 73 - 83
Main Authors Wei, Li, Wu, Ruo-Bin, Yang, Cheng-Min, Zheng, Shao-Yi, Yu, Xi-Yong
Format Journal Article
LanguageEnglish
Published Basel, Switzerland S. Karger AG 01.01.2011
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Summary:Objectives: The etiology of myocardial ischemia/reperfusion (I/R) injury is multifactorial, but activation of the innate immune system and the resulting inflammatory response are important components of I/R injury. The aim of this study was to investigate the protective effect of a hemoglobin-based oxygen carrier (HBOC) on cold I/R heart and to explore the underlying mechanisms. Methods: Isolated Sprague-Dawley rat hearts were perfused in the Langendorff mode. After 30 min of basal perfusion, rat hearts were arrested with histidine-tryptophan-ketoglutarate solution (HTKs) with or without an HBOC and hypothermically stored (4°C) for 9 or 14 h, followed by 2 h of reperfusion. Results: Compared with HTKs alone, the HBOC in HTKs greatly improved heart contraction and decreased infarct size, necrosis and apoptosis, which was related to the reduced expression of Toll-like receptor 2 (TLR 2), TLR 4, TNF-α, IL-1β and nuclear factor-ĸB (NF-ĸB) activation. Conclusions: Our results demonstrated that the HBOC protected isolated rat heart from cold I/R injury and this protection was associated with attenuation of the expression of the TLR 2 and TLR 4/NF-ĸB signaling pathway, which may down-regulate the inflammatory response.
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ISSN:0008-6312
1421-9751
DOI:10.1159/000333106