| Coronary microembolization does not induce acute preconditioning against infarction in pigs-the role of adenosine. | |
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MedLine Citation:
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PMID: 15249189 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: After coronary microembolization (ME) adenosine is released from ischemic areas of the microembolized myocardium. This adenosine dilates vessels in adjacent nonembolized myocardium and increases coronary blood flow. For ischemic preconditioning (IP) to protect the myocardium against infarction, an increase in the interstitial adenosine concentration (iADO) prior to the subsequent ischemia/reperfusion is necessary. We hypothesized that the adenosine release after ME is sufficient to increase iADO and protect the myocardium against infarction from subsequent ischemia/reperfusion. We have therefore compared myocardial protection by either coronary microembolization or ischemic preconditioning prior to ischemia/reperfusion. METHODS: In anesthetized pigs, the left anterior descending (LAD) was cannulated and perfused from an extracorporeal circuit. In 11 pigs, sustained ischemia was induced by 85% inflow reduction for 90 min (controls). Two other groups of pigs were subjected either to IP (n = 8; 10-min ischemia/15-min reperfusion) or coronary ME (n = 9; i.c. microspheres; 42 microm Ø; 3000 x ml(-1) x min inflow) prior to sustained ischemia. Coronary venous adenosine concentration (vADO) and iADO (microdialysis) were measured. Infarct size was determined after 2-h reperfusion by triphenyl tetrazolium chloride staining. RESULTS: In pigs subjected to IP, infarct size was reduced to 2.6 +/- 1.1% (mean +/- S.E.M.) vs. 17.0 +/- 3.2% in controls. iADO was increased from 2.4 +/- 1.3 to 13.1 +/- 5.8 micromol x l(-1) during the reperfusion following IP. In pigs subjected to ME, at 10 min after ME, coronary blood flow (38.6 +/- 3.6 to 53.6 +/- 4.3 ml x min(-1)) and vADO (0.25 +/- 0.04 to 0.48 +/- 0.07 micromol x l(-1)) were increased. However, iADO (2.0 +/- 0.5 at baseline vs. 2.3 +/- 0.6 micromol x l(-1) at 10 min after ME) did not increase. Infarct size induced by sustained ischemia following ME (22.5 +/- 5.2%) was above that of controls for any given subendocardial blood flow. CONCLUSION: ME released adenosine into the vasculature and increased coronary blood flow. The failure of iADO to increase with ME possibly explains the lack of protection against infarction after ME. |
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Authors:
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Andreas Skyschally; Rainer Schulz; Petra Gres; Ina Konietzka; Claus Martin; Michael Haude; Raimund Erbel; Gerd Heusch |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cardiovascular research Volume: 63 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 2004 Aug |
Date Detail:
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Created Date: 2004-07-13 Completed Date: 2004-10-13 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 313-22 Citation Subset: IM |
Copyright Information:
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Copyright 2004 European Society of Cardiology |
Affiliation:
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Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstrasse 55, 45122 Essen, Germany. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine
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metabolism* Animals Coronary Circulation Coronary Stenosis / metabolism* Female Ischemic Preconditioning, Myocardial* Male Models, Animal Myocardial Infarction / metabolism* Myocardium / metabolism* Swine Swine, Miniature Tumor Necrosis Factor-alpha / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Tumor Necrosis Factor-alpha; 58-61-7/Adenosine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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