Difference between revisions of "CH Bern Djafarzadeh S"
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{{MiPNetLab | {{MiPNetLab | ||
|address='''Djafarzadeh Siamak''', Dr. | |address='''[[Djafarzadeh S|Djafarzadeh Siamak]]''', Dr. | ||
Dept. of Intensive Care Medicine (KIM) | Dept. of Intensive Care Medicine (KIM) | ||
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|Info=[http://www.oroboros.at/index.php?id=1217 CH_Bern_DjafarzadehS] | |Info=[http://www.oroboros.at/index.php?id=1217 CH_Bern_DjafarzadehS] | ||
}} | }} | ||
* This lab uses '''3 O2k | * '''[http://www.oroboros.at/?Power-O2k Power-O2k]''': This lab uses '''3 O2k'''. | ||
== Poster presentation == | == Poster presentation == | ||
Revision as of 09:32, 20 April 2012
- Power-O2k: This lab uses 3 O2k.
Poster presentation
SYSTEMIC OXYGEN CONSUMPTION AND MITOCHONDRIAL RESPIRATION ARE MAINTAINED IN LETHAL PORCINE FECAL PERITONITIS
S. Hostettler1, M. Vuda1, T.D. Correa1, S. Djafarzadeh1, J. Takala1, S.M. Jakob1 1Inselspital, University Hospital Bern and University of Bern, Department of Intensive Care Medicine, Bern, Switzerland
ESICM - Berlin 2011 http://poster-consultation.esicm.org/ModuleConsultationPoster/posterDetail.aspx?intIdPoster=3142
INTRODUCTION. Mitochondrial dysfunction has been implicated in sepsis-induced organ failure. OBJECTIVES. To evaluate systemic oxygen consumption (VO2) and skeletal mitochondrial respiration in a lethal model of fecal peritonitis. METHODS. In eight anesthetized pigs [43 ± 2 kg (mean ± SD)], fecal peritonitis was induced by instillation of 2.0 g/kg of autologous feces. Besides infusion of Ringer's lactate and glucose 50% (in total 1.5 mL/kg/h), no resuscitation was performed until death occurred. Cardiac output was measured by thermodilution, and VO2 by indirect calorimetry. At baseline and before death occurred, biopsies of skeletal muscle were obtained, and mitochondrial respiration was measured using high-resolution respirometry (Oxygraph-2k, Oroboros Instruments, Innsbruck, Austria). RESULTS. Death occurred in 21 ± 6 h. Cardiac output and mean arterial pressure decreased (Figure). Arterial lactate concentration increased, but VO2 was maintained and maximal mitochondrial respiration (Complex I, State 3) was enhanced [baseline (median, range): 1320 (1151-1585) pmol/s/mg; end: 1838 (1454-2581) pmol/s/mg, p=0.043, Wilcoxon Test]. The respiratory control ratio (state 3/state 4) remained unchanged [baseline: 9.7 (8.4-12.6); end: 9.3 (7.8-18.3)]. CONCLUSIONS. Despite severely deteriorating hemodynamics and impending death, systemic and skeletal muscle Complex I maximal oxygen consumption were maintained without signs of deteriorated efficiency. In this sepsis model, organ failure and death were not associated with impaired skeletal muscle mitochondrial respiration. GRANT ACKNOWLEDGMENT. This work was supported by the Swiss National Science Foundation (Grant nº 32003B_127619).
Figure: Cardiac output, mean arterial pressure, VO2 and lactate concentrations
Data are shown as mean ± SD. CO, cardiac output; MAP, mean arterial pressure; VO2, systemic oxygen consumption. *Stats: ANOVArm.
