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<art>
   <ui>cc6623</ui>
   <ji>CCJ</ji>
   <fm>
      <dochead>Poster presentation</dochead>
      <bibl>
         <title>
            <p>Glucose metabolism during hyperdynamic septic shock: comparison between noradrenaline and vasopressin</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Hauser</snm>
               <fnm>B</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A2">
               <snm>Giudici</snm>
               <fnm>R</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A3">
               <snm>Simon</snm>
               <fnm>F</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A4">
               <snm>Duy</snm>
               <fnm>C Nguyen</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A5">
               <snm>Radermacher</snm>
               <fnm>P</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A6">
               <snm>Calzia</snm>
               <fnm>E</fnm>
               <insr iid="I1"/>
            </au>
         </aug>
         <insg>
            <ins id="I1">
               <p>Universit&#228;tsklinikum, Ulm, Germany.</p>
            </ins>
         </insg>
         <source>Critical Care</source>
         <supplement>
            <title>
               <p>28th International Symposium on Intensive Care and Emergency Medicine</p>
            </title>
            <note>Meeting abstracts</note>
         </supplement>
         <conference>
            <title>
               <p>28th International Symposium on Intensive Care and Emergency Medicine</p>
            </title>
            <location>Brussels, Belgium</location>
            <date-range>18&#8211;21 March 2008</date-range>
            <url>http://www.intensive.org/</url>
         </conference>
         <issn>1364-8535</issn>
         <pubdate>2008</pubdate>
         <volume>12</volume>
         <issue>Suppl 2</issue>
         <fpage>P402</fpage>
         <url>http://ccforum.com/content/12/S2/P402</url>
         <xrefbib>
            <pubid idtype="doi">10.1186/cc6623</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>13</day>
               <month>3</month>
               <year>2008</year>
            </date>
         </pub>
      </history>
      <cpyrt>
         <year>2008</year>
         <collab>BioMed Central Ltd</collab>
         <note/>
      </cpyrt>
   </fm>
   <bdy>
      <sec>
         <st>
            <p>Introduction</p>
         </st>
         <p>In septic shock, arginine&#8211;vasopressin (AVP) infusion efficiently maintains the mean arterial pressure (MAP), but may compromise hepatosplanchnic perfusion due to excessive vasoconstriction and, thus, depress whole-body and regional substrate metabolism. In this context, the underlying hemodynamic status is crucial <abbrgrp><abbr bid="B1">1</abbr></abbrgrp>. We therefore compared the effects of noradrenaline (NA) and AVP on hepatosplanchnic blood flow, whole body glucose oxidation and hepatic gluconeogenesis during resuscitated, hyperdynamic septic shock.</p>
      </sec>
      <sec>
         <st>
            <p>Methods</p>
         </st>
         <p>After intraperitoneal faeces inoculation <abbrgrp><abbr bid="B2">2</abbr></abbrgrp>, anesthetized, mechanically ventilated and instrumented pigs were randomly assigned to NA (increments of 0.06 &#956;g/kg/min until maximal heart rate of 160/min; <it>n </it>= 8) or AVP (1&#8211;5 ng/kg/min, supplemented by NA if the maximum AVP dosage alone failed to maintain MAP; <it>n </it>= 9) to treat sepsis-associated hypotension. During continuous infusion of stable, nonradioactively labeled 1,2,3,4,5,6-<sup>13</sup>C<sub>6</sub>-glucose, blood isotope (gas chromatography&#8211;mass spectrometry) and expiratory gas <sup>13</sup>CO<sub>2 </sub>(nondispersive infrared spectrometry) enrichment was measured to derive gluconeogenesis and direct aerobic glucose oxidation <abbrgrp><abbr bid="B2">2</abbr></abbrgrp> together with portal venous (Qpv) and hepatic arterial (Qha) blood flows (ultrasound flow probes). Data are the median (quartiles), and <it>P </it>&lt; 0.05 was regarded as significant for AVP versus NA.</p>
      </sec>
      <sec>
         <st>
            <p>Results</p>
         </st>
         <p>At 24 hours of sepsis AVP resulted in significantly lower cardiac output and Qpv (20 (11&#8211;36) vs 26 (15&#8211;35) ml/kg/min), while Qha was comparable (3.0 (0.1&#8211;6.0) vs 2.1 (0.1&#8211;5.1) ml/kg/min). Despite significantly lower NA infusion rates (0.08 (0.0&#8211;0.64) vs 0.56 (0.05&#8211;4.36) &#956;g/kg/min), AVP did not affect the parameters of energy expenditure (O<sub>2 </sub>uptake (5.8 (3.9&#8211;8.1) vs 4.7 (4.2&#8211;6.6) ml/kg/min), CO<sub>2 </sub>production (3.4 (2.3&#8211;4.9) vs 3.5 (2.9&#8211;4.7) ml/kg/min)), nor glucose metabolism (glucose oxidation 3.9 (0.6&#8211;4.6) vs 3.7 (0.6&#8211;4.6) mg/kg/min; gluconeogenesis 6.8 (4.6&#8211;8.5) vs 7.2 (4.9&#8211;11.0) mg/kg/min).</p>
      </sec>
      <sec>
         <st>
            <p>Conclusion</p>
         </st>
         <p>Given the markedly lower NA infusion rates, the unchanged parameters of substrate utilization suggest improved cellular energy metabolism during AVP infusion.</p>
      </sec>
   </bdy>
   <bm>
      <ack>
         <sec>
            <st>
               <p>Acknowledgements</p>
            </st>
            <p>Supported by Ferring Pharmaceuticals A/S and the Deutscher Akademischer Austauschdienst.</p>
         </sec>
      </ack>
      <refgrp>
         <bibl id="B1">
            <aug>
               <au>
                  <snm>Bracht</snm>
                  <fnm>H</fnm>
               </au>
               <etal/>
            </aug>
            <source>Crit Care</source>
            <pubdate>2007</pubdate>
            <volume>11</volume>
            <fpage>178</fpage>
            <xrefbib>
               <pubidlist>
                  <pubid idtype="pmcid">2246204</pubid>
                  <pubid idtype="pmpid" link="fulltext">18177510</pubid>
                  <pubid idtype="doi">10.1186/cc6171</pubid>
               </pubidlist>
            </xrefbib>
         </bibl>
         <bibl id="B2">
            <aug>
               <au>
                  <snm>Barth</snm>
                  <fnm>E</fnm>
               </au>
               <etal/>
            </aug>
            <source>Crit Care Med</source>
            <pubdate>2008</pubdate>
            <volume>36</volume>
            <fpage>495</fpage>
            <lpage>503</lpage>
            <xrefbib>
               <pubid idtype="pmpid" link="fulltext">18091553</pubid>
            </xrefbib>
         </bibl>
      </refgrp>
   </bm>
</art>

