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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/BF02616286</subfield>
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   <subfield code="a">Influence of ischemic preconditioning and blood cardioplegia protection on postischemic endothelial activation in coronary bypass surgery</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[G. Steinhoff, M. Karck, J. Cremer, T. Ahnsel, D. Hollander, A. Haverich]</subfield>
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   <subfield code="a">Einfluß von ischämischer Präkonditionierung und Blutkardioplegieprotektion auf die postischämische Endothelaktivierung in der Koronarchirurgie</subfield>
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   <subfield code="a">Summary: Background: Hypothermic ischemia in open heart surgery and cardiopulmonary bypass involve a postischemic in-flammatory reaction caused by an activation of leukocytes and endothelia with the systemic release of cytokines and adhesion molecules. The present study addresses the question, if an amelioration of postischemic endothelial activation in the heart could be achieved by means of cardioplegic protection or ischemic preconditioning. In a randomized prospective study patients underwent a normothermic preconditioning procedure either followed by crystalloid or blood cardioplegia during coronary bypass surgery. Methods: Patients (n=28) were included and randomized in the study according to defined criteria: Group A received St. Thomas cardioplegia, group B cold blood cardioplegia. Ischemic precon-ditioning was performed twice at normothermia under a cardiopulmonary bypass (CPB) for 5 min followed by 10 min of reperfusion before coronary aortic bypass graft (CABG) using St. Thomas (group C) or blood cardioplegia (group D) hypothermic protection. In coronary sinus blood and arterial blood myocardial (creatine-kinase myoglobin [CK-MB]) and endothelial activation (endothelin, IL-6, IL-8, sE-selectin, soluble vascular adhesion molecule-1 [sVCAM-1], soluble intercellular adhesion molecule-1 [sICAM-1]) parameters were investigated 1, 3, 6, 9, 12, and 24 h after coronary reperfusion. Results: 1) Parameters of myocardial injury (CK-MB, myoglobin) revealed increased levels at 1 h and 9 to 12 h after CABG. Levels at 12 h were lower in group B and D as compared to A and C. 2) Cytokines (IL-6, IL-8) showed increased levels 3 h after reperfusion with no difference between study groups. 3) Soluble adhesion molecules (E-selectin, VCAM-1, ICAM-1) were found increased in all groups 6 to 12 h after reperfusion. Lower levels were present in group D for E-selectin and VCAM-1. Conclusions: The results indicate a sequence of cytokine and adhesion molecule release as a potential pathomechanism of myocardial reperfusion injury. Gradual decrease in the release of endothelial adhesion molecules in late myocardial injury was noted for blood cardioplegia and ischemic preconditioning. Amelioration of endothelial activation by means of preconditioning and blood cardioplegia may improve heart muscle recovery in open heart surgery with borderline ischemia time and organ dysfunction.</subfield>
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  <datafield tag="540" ind1=" " ind2=" ">
   <subfield code="a">Blackwell Science Ltd, 1996</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Cytokines</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">soluble adhesion molecules</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">reperfusion injury</subfield>
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   <subfield code="a">coronary bypass surgery</subfield>
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   <subfield code="a">ischemic preconditioning</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">blood cardioplegia</subfield>
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   <subfield code="a">Zytokine</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">lösliche Adhäsionsmoleküle</subfield>
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   <subfield code="a">Reperfusionsschaden</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Koronarchirurgie</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">ischämische Präkonditionierung</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Blut-Kardioplegie</subfield>
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   <subfield code="a">Steinhoff</subfield>
   <subfield code="D">G.</subfield>
   <subfield code="u">Department of Heart and Vascular Surgery, University Kiel, Germany</subfield>
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   <subfield code="a">Karck</subfield>
   <subfield code="D">M.</subfield>
   <subfield code="u">Department of Heart and Vascular Surgery, University Kiel, Germany</subfield>
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   <subfield code="a">Cremer</subfield>
   <subfield code="D">J.</subfield>
   <subfield code="u">Department of Heart and Vascular Surgery, University Kiel, Germany</subfield>
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   <subfield code="u">Department of Heart and Vascular Surgery, University Kiel, Germany</subfield>
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   <subfield code="u">Department of Heart and Vascular Surgery, University Kiel, Germany</subfield>
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   <subfield code="t">Acta Chirurgica Austriaca</subfield>
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   <subfield code="g">28/6(1996-12-01), 354-358</subfield>
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