Impairment of exogenous lactate clearance in experimental hyperdynamic septic shock is not related to total liver hypoperfusion

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dc.contributor.authorTapia Ossa, Pablo José
dc.contributor.authorSoto, Dagoberto
dc.contributor.authorBruhn, Alejandro
dc.contributor.authorAlegría, Leyla
dc.contributor.authorJarufe Cassis, Nicolás
dc.contributor.authorKattan Tala, Eduardo José
dc.contributor.authorRegueira Heskia, Tomás
dc.contributor.authorMeissner, Arturo
dc.contributor.authorMenchaca, Rodrigo
dc.contributor.authorVives, María Ignacia
dc.date.accessioned2019-10-17T13:18:22Z
dc.date.available2019-10-17T13:18:22Z
dc.date.issued2014
dc.date.updated2019-10-14T19:04:57Z
dc.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.
dc.fuente.origenBiomed Central
dc.identifier.citationCritical Care. 2015 Apr 22;19(1):188
dc.identifier.doi10.1186/s13054-015-0928-3
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/26617
dc.issue.numeroNo. 188
dc.language.isoen
dc.pagina.final10
dc.pagina.inicio1
dc.revistaCritical Carees_ES
dc.rights.holderTapia et al.; licensee BioMed Central.
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.otherEnfermedades hepáticases_ES
dc.subject.otherHiperlipemiaes_ES
dc.subject.otherChoque sépticoes_ES
dc.titleImpairment of exogenous lactate clearance in experimental hyperdynamic septic shock is not related to total liver hypoperfusiones_ES
dc.typeartículo
dc.volumenVol. 19
sipa.codpersvinculados741
sipa.codpersvinculados104492
sipa.codpersvinculados18434
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