Correa 2014 Crit Care Med: Difference between revisions
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{{Publication | {{Publication | ||
|title=CorrΓͺa TD, Jeger V, Pereira AJ, Takala J, Djafarzadeh S, Jakob SM (2014) Angiotensin II in | |title=CorrΓͺa 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. | ||
|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 | ||
}} | }} | ||
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|organism=Pig | |organism=Pig | ||
|tissues=Heart, Liver, Kidney | |tissues=Heart, Liver, Kidney | ||
|preparations=Permeabilized tissue, Isolated | |preparations=Permeabilized tissue, Isolated mitochondria | ||
|diseases=Sepsis | |diseases=Sepsis | ||
|couplingstates=LEAK, OXPHOS | |couplingstates=LEAK, OXPHOS | ||
| | |pathways=N, S, CIV, NS | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Latest revision as of 16:06, 7 November 2016
CorrΓͺa 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. |
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.
β’ O2k-Network Lab: CH Bern Djafarzadeh S
Labels: MiParea: Respiration
Pathology: Sepsis
Organism: Pig Tissue;cell: Heart, Liver, Kidney Preparation: Permeabilized tissue, Isolated mitochondria
Coupling state: LEAK, OXPHOS
Pathway: N, S, CIV, NS
HRR: Oxygraph-2k