<?xml version='1.0'?>
<!DOCTYPE art SYSTEM 'http://www.biomedcentral.com/xml/article.dtd'>
<art>
   <ui>cc320</ui>
   <ji>CCJ</ji>
   <fm>
      <dochead>Meeting abstract</dochead>
      <bibl>
         <title>
            <p>Regulation of platelet-leukocyte interaction in simulated ECC: attenuation with heparin surface modification</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Schmid</snm>
               <fnm>F-X</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A2">
               <snm>Choi</snm>
               <fnm>YH</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A3">
               <snm>Zhou</snm>
               <fnm>X</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A4">
               <snm>Hilker</snm>
               <fnm>M</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A5">
               <snm>Habermehl</snm>
               <fnm>P</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A6">
               <snm>Zepp</snm>
               <fnm>F</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A7">
               <snm>Oelert</snm>
               <fnm>H</fnm>
               <insr iid="I1"/>
            </au>
         </aug>
         <insg>
            <ins id="I1">
               <p>Department of Cardiothoracic Surgery, University Hospitals, D-55101 Mainz, Germany</p>
            </ins>
         </insg>
         <source>Critical Care</source>
         <supplement>
            <title>
               <p>International Symposium on the Pathophysiology of Cardiopulmonary Bypass</p>
            </title>
            <note>Meeting abstracts</note>
         </supplement>
         <conference>
            <title>
               <p>International Symposium on the Pathophysiology of Cardiopulmonary Bypass</p>
            </title>
            <location>Aachen, Germany</location>
            <date-range>12 December 1998</date-range>
         </conference>
         <issn>1364-8535</issn>
         <pubdate>1999</pubdate>
         <volume>3</volume>
         <issue>Suppl A</issue>
         <fpage>P09</fpage>
         <xrefbib>
            <pubid idtype="doi">10.1186/cc320</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>2</day>
               <month>3</month>
               <year>1999</year>
            </date>
         </pub>
      </history>
      <cpyrt>
         <year>1999</year>
         <collab>Current Science Ltd</collab>
      </cpyrt>
   </fm>
   <meta>
      <classifications>
         <classification type="BMC" subtype="old_arx_id">cc-3-2-p001-p09</classification>
      </classifications>
   </meta>
   <bdy>
      <sec>
         <st>
            <p>Background</p>
         </st>
         <p>Blood exposure to artificial surfaces results in blood cell activation. The present study analyses the impact of heparin immobilisation in a model of simulated extracorporeal circulation SECC on leukocyte and platelet activation, expression of surface markers and adhesion receptors, as well as on leukocyte-platelet interaction.</p>
      </sec>
      <sec>
         <st>
            <p>Methods</p>
         </st>
         <p>Fresh heparinized human blood was recirculated in <it>in vitro</it> cardiopulmonary bypass circuits (untreated: <it>n</it> = 10; coated <it>n</it> = 10; randomized, blinded for group affiliation). Samples were taken before and 15, 30, 60, 120, and 180 min after commencement of circulation. By means of flow cytometry neutrophil activation (respiratory burst; expression of CD11b), platelet activation (GpIb and GMP140 expression), as well as numbers of monocytes/PMNs binding platelets were assessed.</p>
      </sec>
      <sec>
         <st>
            <p>Results</p>
         </st>
         <p>Blood cell activation and interaction demonstrated ECC-dependent dynamics. SECC produced significant PMN activation and platelet GMP140 expression. Monocytes bound more platelets and at an faster rate than PMNs. In the group with heparin-coated surfaces PMN activation was significantly reduced, GMP140 expression less upregulated and leukocyte-platelet adhesion diminished.</p>
      </sec>
      <sec>
         <st>
            <p>Conclusions</p>
         </st>
         <p>Heparin coating in SECC reduces neutrophil and platelet activation and attenuates leukocyte-platelet adhesion. These studies indicate that there are cross-links between hemostatic and inflammatory disorders associated with ECC.</p>
      </sec>
   </bdy>
</art>
