Apyrase treatment of myocardial infarction according to a clinically applicable protocol fails to reduce myocardial injury in a porcine model

BMC Cardiovascular Disorders

Research Article

Jesper van der Pals¹  Michael I Götberg¹  Sasha Koul¹  Matthias Götberg¹  Göran K Olivecrona¹  David Erlinge¹  Mikael Kanski²  Martin Ugander²  Håkan Arheden²  Andreas Otto² 

[1] Department of Cardiology, Lund University Hospital, Lund, Sweden;Department of Clinical Physiology, Lund University Hospital, Lund, Sweden;

关键词: Single Photon Emission Compute Tomography;    Infarct Size;    Left Anterior Descend;    Base Excess;    Single Photon Emission Compute Tomography Image;   

DOI  :  10.1186/1471-2261-10-1

 received in 2009-10-08, accepted in 2010-01-04,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundEctonucleotidase dependent adenosine generation has been implicated in preconditioning related cardioprotection against ischemia-reperfusion injury, and treatment with a soluble ectonucleotidase has been shown to reduce myocardial infarct size (IS) when applied prior to induction of ischemia. However, ectonucleotidase treatment according to a clinically applicable protocol, with administration only after induction of ischemia, has not previously been evaluated. We therefore investigated if treatment with the ectonucleotidase apyrase, according to a clinically applicable protocol, would reduce IS and microvascular obstruction (MO) in a large animal model.MethodsA percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 min, in 16 anesthetized pigs (40-50 kg). The pigs were randomized to 40 min of 1 ml/min intracoronary infusion of apyrase (10 U/ml, n = 8) or saline (0.9 mg/ml, n = 8), twenty minutes after balloon inflation. Area at risk (AAR) was evaluated by ex vivo SPECT. IS and MO were evaluated by ex vivo MRI.ResultsNo differences were observed between the apyrase group and saline group with respect to IS/AAR (75.7 ± 4.2% vs 69.4 ± 5.0%, p = NS) or MO (10.7 ± 4.8% vs 11.4 ± 4.8%, p = NS), but apyrase prolonged the post-ischemic reactive hyperemia.ConclusionApyrase treatment according to a clinically applicable protocol, with administration of apyrase after induction of ischemia, does not reduce myocardial infarct size or microvascular obstruction.

【 授权许可】

Unknown   
© van der Pals et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.