CH Bern Djafarzadeh S

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CH Bern Djafarzadeh S

Oroboros O2k-Network

O2k-Network
O2k-Network Lab Department of Intensive Care Medicine (KIM)

Universitätsspital Bern (Inselspital)

Address Freiburgstasse Pav. 52B, CH-3010
City Bern
State/Prov
Country Switzerland
Weblink
Contact Djafarzadeh Siamak
Team Bhaskar Monica, Nansoz Sandra
Team previous Jeger Victor, Lepper Philipp M, Regueira Thomas, Vuda Madhusudanarao, Wyss Rahel
Status 3 Power-O2k 2006-
Oroboros Events IOC116, IOC109, IOC66, IOC54, IOC36
Topics


O2k-Publications

 PublishedReference
Correa 2017 Crit Care2017Corrêa TD, Pereira AJ, Brandt S, Vuda M, Djafarzadeh S, Takala J, Jakob SM (2017) Time course of blood lactate levels, inflammation, and mitochondrial function in experimental sepsis. Crit Care 21:105.
Djafarzadeh 2017b J Vis Exp2017Djafarzadeh S, Jakob SM (2017) Isolation of intact mitochondria from skeletal muscle by differential centrifugation for High-Resolution Respirometry measurements. J Vis Exp doi: 10.3791/55251.
Djafarzadeh 2017 J Vis Exp2017Djafarzadeh S, Jakob SM (2017) High-resolution respirometry to assess mitochondrial function in permeabilized and intact cells. J Vis Exp 8.doi: 10.3791/54985..
Spendiff 2016 J Physiol2016Spendiff S, Vuda M, Gouspillou G, Aare S, Perez A, Morais JA, Jagoe RT, Filion ME, Glicksman R, Kapchinsky S, MacMillan NJ, Pion CH, Aubertin-Leheudre M, Hettwer S, Correa JA, Taivassalo T, Hepple RT (2016) Denervation drives mitochondrial dysfunction in skeletal muscle of octogenarians. J Physiol 594:7361-79.
Jeger 2015 BioMed Res Internat2015Jeger V, Brandt S, Porta F, Jakob SM, Takala J, Djafarzadeh S (2015) Dose response of Endotoxin on hepatocyte and muscle mitochondrial respiration in vitro. BioMed Res Internat Article ID 353074:1-13.
Tapia 2015 Crit Care2015Tapia P, Soto D, Bruhn A, Alegría L, Jarufe N, Luengo C, Kattan E, Regueira T, Meissner A, Menchaca R, Vives MI, Echeverría N, Ospina-Tascón G, Bakker J, Hernández G (2015) Impairment of exogenous lactate clearance in experimental hyperdynamic septic shock is not related to total liver hypoperfusion. Crit Care 19:188.
Correa 2014 Crit Care Med2014Corrêa TD, Jeger V, Pereira AJ, Takala J, Djafarzadeh S, Jakob SM (2014) Angiotensin II in septic shock: effects on tissue perfusion, organ function, and mitochondrial respiration in a porcine model of fecal peritonitis. Crit Care Med 42:e550-9.
Jeger 2013 Abstracts of ESICM LIVES 20132013Jeger V, Steinmann M, Takala J, Jakob SM, Djafarzadeh S (2013) TLR-2-induced mitochondrial dysfunction in cultured human hepatocytes. Abstracts of ESICM LIVES 2013
Correa 2013 Crit Care2013Corrêa TD, Vuda M, Takala J, Djafarzadeh S, Silva E, Jakob SM (2013) Increasing mean arterial blood pressure in sepsis: effects on fluid balance, vasopressor load and renal function. Crit Care 17:R21.
Astin 2013 Sci Rep2013Astin R, Bentham R, Djafarzadeh S, Horscroft JA, Kuc RE, Leung PS, Skipworth JR, Vicencio JM, Davenport AP, Murray AJ, Takala J, Jakob SM, Montgomery H, Szabadkai G (2013) No evidence for a local renin-angiotensin system in liver mitochondria. Sci Rep 3:2467.
Djafarzadeh 2012 PLoS One2012Djafarzadeh S, Vuda M, Takala J, Jakob SM (2012) Effect of remifentanil on mitochondrial oxygen consumption of cultured human hepatocytes. PLoS One 7:e45195.
Chiusa 2012 J Mol Cell Cardiol2012Chiusa M, Hool SL, Truetsch P, Djafarzadeh S, Jakob SM, Seifriz F, Scherer SJ, Suter TM, Zuppinger C, Zbinden S (2012) Cancer therapy modulates VEGF signaling and viability in adult rat cardiac microvascular endothelial cells and cardiomyocytes. J Mol Cell Cardiol 52:1164-75.
Correa 2012 Crit Care Med2012Corrêa TD, Vuda M, Blaser AR, Takala J, Djafarzadeh S, Dünser MW, Silva E, Lensch M, Wilkens L, Jakob SM (2012) Effect of treatment delay on disease severity and need for resuscitation in porcine fecal peritonitis. Crit Care Med 40:2841-9.
Vuda 2012 Innate Immun2012Vuda M, Brander L, Schröder R, Jakob SM, Takala J, Djafarzadeh S (2012) Effects of catecholamines on hepatic and skeletal muscle mitochondrial respiration after prolonged exposure to faecal peritonitis in pigs. Innate Immun 18:217-30.
Djafarzadeh 2011 Mitochondrion2011Djafarzadeh S, Vuda M, Takala J, Ochs M, Jakob SM (2011) Toll-like receptor-3-induced mitochondrial dysfunction in cultured human hepatocytes. Mitochondrion 11:83-8.
Spirig 2010 PLoS One2010Spirig R, Djafarzadeh S, Regueira T, Shaw SG, von Garnier C, Takala J, Jakob SM, Rieben R, Lepper PM (2010) Effects of TLR agonists on the hypoxia-regulated transcription factor HIF-1alpha and dendritic cell maturation under normoxic conditions. PLoS One 5:e0010983.
Regueira 2009 Liver Int2009Regueira T, Lepper PM, Brandt S, Ochs M, Vuda M, Takala J, Jakob SM, Djafarzadeh S (2009) Hypoxia inducible factor-1alpha induction by tumour necrosis factor-alpha, but not by toll-like receptor agonists, modulates cellular respiration in cultured human hepatocytes. Liver Int 10:1582-92.
Regueira 2008 Crit Care Med2008Regueira T, Baenziger B, Djafarzadeh S, Brandt S, Gorrasi J, Takala J, Lepper PM, Jakob SM (2008) Norepinephrine to increase blood pressure in endotoxaemic pigs is associated with improved hepatic mitochondrial respiration. Crit Care Med 12:R88

O2k-Abstracts

update please

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.

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* We are really satisfied with the O2k and we hope to measure mitochondrial membrane potential ASAP. - Siamak Djafarzadeh (2011)