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Título : Angiotensin II in septic shock: effects on tissue perfusion, organ function, and mitochondrial respiration in a porcine model of fecal peritonitis
Autor: Corrêa, Thiago D.
Jeger, Victor
Pereira, Adriano José
Takala, Jukka
Djafarzadeh, Siamak
Jakob, Stephan M.
Palavras-chave: Septic shock
Angiotensin II – Therapeutic use
Norepinephrine - Therapeutic use
Swine as laboratory animals
Choque séptico
Angiotensina II – Uso terapêutico
Norepinefrina - Uso terapêutico
Suíno como animal de laboratório
Publicador: Williams & Wilkins
Data da publicação: 2014
Referência: CORRÊA, T. D. et al. Angiotensin II in septic shock: effects on tissue perfusion, organ function, and mitochondrial respiration in a porcine model of fecal peritonitis. Critical Care Medicine, Baltimore, v. 42, n. 8, p. e550-e559, Aug 2014.
Abstract: Objectives: To compare effects of norepinephrine and angiotensin II in experimental sepsis on hemodynamics, organ function, and mitochondrial respiration. 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 (75–85mm Hg) was reached in both NE and AT-II, and ­cardiac output increased similarly (NE: from 64mL/kg/min [60–79mL/kg/min] to 139mL/kg/min [126–157mL/kg/min]; AT-II from 79mL/kg/min [65–86mL/kg/min] to 145mL/kg/min [126–147mL/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: 81mm Hg [76–85mm Hg]; AT-II: 80mm Hg [77–84mm Hg]; E: 53mm Hg [49–66mm 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.
URI: http://ovidsp.tx.ovid.com/sp-3.20.0b/ovidweb.cgi?QS2=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
http://repositorio.ufla.br/jspui/handle/1/12360
Idioma: en_US
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