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Authordc.contributor.authorTapia, Pablo 
Authordc.contributor.authorSoto, Dagoberto 
Authordc.contributor.authorBruhn, Alejandro 
Authordc.contributor.authorAlegría, Leyla 
Authordc.contributor.authorJarufe, Nicolás 
Authordc.contributor.authorLuengo Messen, Cecilia 
Authordc.contributor.authorKattan, Eduardo 
Authordc.contributor.authorRegueira, Tomás 
Authordc.contributor.authorMeissner, Arturo 
Authordc.contributor.authorMenchaca, Rodrigo 
Authordc.contributor.authorVives, María Ignacia 
Authordc.contributor.authorEcheverría, Nicolas 
Authordc.contributor.authorOspina Tascón, Gustavo 
Authordc.contributor.authorBakker, Jan 
Authordc.contributor.authorHernández, Glenn 
Cita de ítemdc.identifier.citationCritical Care (2015) 19:188en_US
Identifierdc.identifier.otherDOI 10.1186/s13054-015-0928-3
General notedc.descriptionArtículo de publicación ISIen_US
Abstractdc.description.abstractIntroduction: Although the prognostic value of persistent hyperlactatemia in septic shock is unequivocal, its physiological determinants are controversial. Particularly, the role of impaired hepatic clearance has been underestimated and is only considered relevant in patients with liver ischemia or cirrhosis. Our objectives were to establish whether endotoxemia impairs whole body net lactate clearance, and to explore a potential role for total liver hypoperfusion during the early phase of septic shock. Methods: After anesthesia, 12 sheep were subjected to hemodynamic/perfusion monitoring including hepatic and portal catheterization, and a hepatic ultrasound flow probe. After stabilization (point A), sheep were alternatively assigned to lipopolysaccharide (LPS) (5 mcg/kg bolus followed by 4 mcg/kg/h) or sham for a three-hour study period. After 60 minutes of shock, animals were fluid resuscitated to normalize mean arterial pressure. Repeated series of measurements were performed immediately after fluid resuscitation (point B), and one (point C) and two hours later (point D). Monitoring included systemic and regional hemodynamics, blood gases and lactate measurements, and ex-vivo hepatic mitochondrial respiration at point D. Parallel exogenous lactate and sorbitol clearances were performed at points B and D. Both groups included an intravenous bolus followed by serial blood sampling to draw a curve using the least squares method. Results: Significant hyperlactatemia was already present in LPS as compared to sham animals at point B (4.7 (3.1 to 6.7) versus 1.8 (1.5 to 3.7) mmol/L), increasing to 10.2 (7.8 to 12.3) mmol/L at point D. A significant increase in portal and hepatic lactate levels in LPS animals was also observed. No within-group difference in hepatic DO2, VO2 or O2 extraction, total hepatic blood flow (point D: 915 (773 to 1,046) versus 655 (593 to 1,175) ml/min), mitochondrial respiration, liver enzymes or sorbitol clearance was found. However, there was a highly significant decrease in lactate clearance in LPS animals (point B: 46 (30 to 180) versus 1,212 (743 to 2,116) ml/min, P <0.01; point D: 113 (65 to 322) versus 944 (363 to 1,235) ml/min, P <0.01). Conclusions: Endotoxemia induces an early and severe impairment in lactate clearance that is not related to total liver hypoperfusion.en_US
Patrocinadordc.description.sponsorshipFONDECYT Chile Grant project number 1130200en_US
Publisherdc.publisherBioMed Centralen_US
Type of licensedc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile*
Link to Licensedc.rights.uri*
Títulodc.titleImpairment of exogenous lactate clearance in experimental hyperdynamic septic shock is not related to total liver hypoperfusionen_US
Document typedc.typeArtículo de revistaen_US

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Except where otherwise noted, this item's license is described as Atribución-NoComercial-SinDerivadas 3.0 Chile