Difference between revisions of "Correa 2014 Crit Care Med"
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{{Publication | {{Publication | ||
|title=Corrêa 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 [Epub ahead of print]. | |title=Corrêa 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 [Epub ahead of print]. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/24797374 PMKID: 24797374] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/24797374 PMKID: 24797374] | ||
|authors=Correa TD, Jeger V, Pereira AJ, Takala J, Djafarzadeh S, Jakob SM | |authors=Correa TD, Jeger V, Pereira AJ, Takala J, Djafarzadeh S, Jakob SM | ||
|year=2014 | |year=2014 | ||
|journal=Crit Care Med | |journal=Crit Care Med | ||
|abstract=OBJECTIVES | |abstract=OBJECTIVES: | ||
To compare effects of norepinephrine and angiotensin II in experimental sepsis on hemodynamics, organ function, and mitochondrial respiration. | To compare effects of norepinephrine and angiotensin II in experimental sepsis on hemodynamics, organ function, and mitochondrial respiration. | ||
DESIGN | DESIGN: | ||
Randomized, controlled, study. | Randomized, controlled, study. | ||
SETTING | SETTING: | ||
University experimental laboratory. | University experimental laboratory. | ||
SUBJECTS | SUBJECTS: | ||
Twenty-eight anesthetized, mechanically ventilated pigs. | Twenty-eight anesthetized, mechanically ventilated pigs. | ||
INTERVENTIONS | INTERVENTIONS: | ||
Sixteen pigs were randomized to receive after 12 hours of fecal peritonitis fluid resuscitation and either norepinephrine (group NE; n = 8) or angiotensin II (group AT-II; n = 8) for 48 hours. A separate group (n = 8), treated with enalapril for 1 week before peritonitis and until study end, received fluids and norepinephrine (group E). The blood pressure dose-response to angiotensin II was evaluated in additional four nonseptic pigs. | Sixteen pigs were randomized to receive after 12 hours of fecal peritonitis fluid resuscitation and either norepinephrine (group NE; n = 8) or angiotensin II (group AT-II; n = 8) for 48 hours. A separate group (n = 8), treated with enalapril for 1 week before peritonitis and until study end, received fluids and norepinephrine (group E). The blood pressure dose-response to angiotensin II was evaluated in additional four nonseptic pigs. | ||
MEASUREMENTS AND MAIN RESULTS | MEASUREMENTS AND MAIN RESULTS: | ||
Blood pressure target (75-85 mm Hg) was reached in both NE and AT-II, and cardiac output increased similarly (NE: from 64 mL/kg/min [60-79 mL/kg/min] to 139 mL/kg/min [126-157 mL/kg/min]; AT-II from 79 mL/kg/min [65-86 mL/kg/min] to 145 mL/kg/min [126-147 mL/kg/min]; median, interquartile range). Renal plasma flow, prevalence of acute kidney injury, inflammation and coagulation patterns, and mitochondrial respiration did not differ between NE and AT-II. In group E, blood pressure targets were not achieved (mean arterial pressure at study end: NE: 81 mm Hg [76-85 mm Hg]; AT-II: 80 mm Hg [77-84 mm Hg]; E: 53 mm Hg [49-66 mm Hg], p = 0.002, compared to NE), whereas skeletal muscle adenosine triphosphate concentrations were increased. During resuscitation one animal died in groups AT-II and E. | Blood pressure target (75-85 mm Hg) was reached in both NE and AT-II, and cardiac output increased similarly (NE: from 64 mL/kg/min [60-79 mL/kg/min] to 139 mL/kg/min [126-157 mL/kg/min]; AT-II from 79 mL/kg/min [65-86 mL/kg/min] to 145 mL/kg/min [126-147 mL/kg/min]; median, interquartile range). Renal plasma flow, prevalence of acute kidney injury, inflammation and coagulation patterns, and mitochondrial respiration did not differ between NE and AT-II. In group E, blood pressure targets were not achieved (mean arterial pressure at study end: NE: 81 mm Hg [76-85 mm Hg]; AT-II: 80 mm Hg [77-84 mm Hg]; E: 53 mm Hg [49-66 mm Hg], p = 0.002, compared to NE), whereas skeletal muscle adenosine triphosphate concentrations were increased. During resuscitation one animal died in groups AT-II and E. | ||
CONCLUSIONS | CONCLUSIONS: | ||
Angiotensin II reversed sepsis-induced hypotension with systemic and regional hemodynamic effects similar to those of norepinephrine. Inhibition of angiotensin-converting enzyme before sepsis worsened the hypotension but enhanced skeletal muscle adenosine triphosphate. Modifying the renin-angiotensin system in sepsis should be further evaluated. | Angiotensin II reversed sepsis-induced hypotension with systemic and regional hemodynamic effects similar to those of norepinephrine. Inhibition of angiotensin-converting enzyme before sepsis worsened the hypotension but enhanced skeletal muscle adenosine triphosphate. Modifying the renin-angiotensin system in sepsis should be further evaluated. | ||
|mipnetlab=CH Bern Djafarzadeh S | |mipnetlab=CH Bern Djafarzadeh S | ||
Revision as of 12:05, 5 June 2014
| Corrêa 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 [Epub ahead of print]. |
Correa TD, Jeger V, Pereira AJ, Takala J, Djafarzadeh S, Jakob SM (2014) Crit Care Med
Abstract: OBJECTIVES: To compare effects of norepinephrine and angiotensin II in experimental sepsis on hemodynamics, organ function, and mitochondrial respiration.
DESIGN: Randomized, controlled, study.
SETTING: University experimental laboratory.
SUBJECTS: Twenty-eight anesthetized, mechanically ventilated pigs.
INTERVENTIONS: Sixteen pigs were randomized to receive after 12 hours of fecal peritonitis fluid resuscitation and either norepinephrine (group NE; n = 8) or angiotensin II (group AT-II; n = 8) for 48 hours. A separate group (n = 8), treated with enalapril for 1 week before peritonitis and until study end, received fluids and norepinephrine (group E). The blood pressure dose-response to angiotensin II was evaluated in additional four nonseptic pigs.
MEASUREMENTS AND MAIN RESULTS: Blood pressure target (75-85 mm Hg) was reached in both NE and AT-II, and cardiac output increased similarly (NE: from 64 mL/kg/min [60-79 mL/kg/min] to 139 mL/kg/min [126-157 mL/kg/min]; AT-II from 79 mL/kg/min [65-86 mL/kg/min] to 145 mL/kg/min [126-147 mL/kg/min]; median, interquartile range). Renal plasma flow, prevalence of acute kidney injury, inflammation and coagulation patterns, and mitochondrial respiration did not differ between NE and AT-II. In group E, blood pressure targets were not achieved (mean arterial pressure at study end: NE: 81 mm Hg [76-85 mm Hg]; AT-II: 80 mm Hg [77-84 mm Hg]; E: 53 mm Hg [49-66 mm Hg], p = 0.002, compared to NE), whereas skeletal muscle adenosine triphosphate concentrations were increased. During resuscitation one animal died in groups AT-II and E.
CONCLUSIONS: Angiotensin II reversed sepsis-induced hypotension with systemic and regional hemodynamic effects similar to those of norepinephrine. Inhibition of angiotensin-converting enzyme before sepsis worsened the hypotension but enhanced skeletal muscle adenosine triphosphate. Modifying the renin-angiotensin system in sepsis should be further evaluated.
• O2k-Network Lab: CH Bern Djafarzadeh S
Labels: MiParea: Respiration
Pathology: Sepsis
Organism: Pig Tissue;cell: Heart, Liver, Kidney Preparation: Permeabilized tissue, Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Coupling state: LEAK, OXPHOS
HRR: Oxygraph-2k
