SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK
Autor(a) principal: | |
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Data de Publicação: | 2011 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/33723 http://dx.doi.org/10.1097/SHK.0b013e3182115e6a |
Resumo: | Severe sepsis is frequently associated with microcirculatory abnormalities despite seemingly adequate hemodynamic resuscitation. As increased serum angiotensin II levels may play a role in this dysfunction, we evaluated the microcirculatory effects of enalaprilat in an experimental model of septic shock. One hour after injection of 1.5 g/kg body weight of feces into the abdominal cavity, 16 adult female anesthetized, mechanically ventilated sheep were randomized to receive 2.5 mg enalaprilat or saline. When fluid-resistant hypotension (mean arterial pressure, <65 mmHg) developed, norepinephrine was given up to a maximal dose of 3 mu g.kg(-1).min(-1). the sublingual microcirculation was evaluated using sidestream dark-field videomicroscopy. A cutoff of 20 mu m was used to differentiate small and large vessels. Experiments were pursued until the sheep's spontaneous death or for a maximum of 30 h. There were progressive and significant reductions in the proportion of small perfused vessels and in the microvascular flow index for small vessels (both P < 0.01 for trend) during shock and the first 2 h of norepinephrine infusion in the placebo group, which were prevented by the administration of enalaprilat. There were no differences between treated and placebo groups in global hemodynamic variables, time to shock or median survival time (21.8 [18.6-28.8] vs. 22.9 [21.8-30.0] h; P = 0.45). However, oxygen exchange was worse (PaO(2)/FIO(2) ratio, 224 [128-297] vs. 332 [187-450]; P < 0.05), and creatinine concentrations increased more in the treated group (from 0.51 [0.42-0.75] to 1.19 [0.64-1.50] mg.dL(-1); P = 0.04) than in the control group (from 0.55 [0.45-0.62] to 0.78 [0.46-1.78] mg.dL(-1); P = 0.12), Enalaprilat therefore prevented the worsening of sublingual microcirculatory variables in this fluid-resuscitated, hyperdynamic model of septic shock, without significant effect on arterial pressure, but with a possible deleterious effect on renal and lung function. |
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Salgado, Diamantino RibeiroHe, XinrongSu, FuhongSousa, Dalton Barros dePenaccini, LauraMaciel, Leonardo KfuriTaccone, FabioRocco, Jose RodolfoSilva, Eliezer [UNIFESP]De Backer, DanielVincent, Jean-LouisUniv Libre BruxellesUniversidade Federal do Rio de Janeiro (UFRJ)Universidade Federal de São Paulo (UNIFESP)Albert Einstein Hosp2016-01-24T14:16:47Z2016-01-24T14:16:47Z2011-06-01Shock. Philadelphia: Lippincott Williams & Wilkins, v. 35, n. 6, p. 542-549, 2011.1073-2322http://repositorio.unifesp.br/handle/11600/33723http://dx.doi.org/10.1097/SHK.0b013e3182115e6a10.1097/SHK.0b013e3182115e6aWOS:000290662700002Severe sepsis is frequently associated with microcirculatory abnormalities despite seemingly adequate hemodynamic resuscitation. As increased serum angiotensin II levels may play a role in this dysfunction, we evaluated the microcirculatory effects of enalaprilat in an experimental model of septic shock. One hour after injection of 1.5 g/kg body weight of feces into the abdominal cavity, 16 adult female anesthetized, mechanically ventilated sheep were randomized to receive 2.5 mg enalaprilat or saline. When fluid-resistant hypotension (mean arterial pressure, <65 mmHg) developed, norepinephrine was given up to a maximal dose of 3 mu g.kg(-1).min(-1). the sublingual microcirculation was evaluated using sidestream dark-field videomicroscopy. A cutoff of 20 mu m was used to differentiate small and large vessels. Experiments were pursued until the sheep's spontaneous death or for a maximum of 30 h. There were progressive and significant reductions in the proportion of small perfused vessels and in the microvascular flow index for small vessels (both P < 0.01 for trend) during shock and the first 2 h of norepinephrine infusion in the placebo group, which were prevented by the administration of enalaprilat. There were no differences between treated and placebo groups in global hemodynamic variables, time to shock or median survival time (21.8 [18.6-28.8] vs. 22.9 [21.8-30.0] h; P = 0.45). However, oxygen exchange was worse (PaO(2)/FIO(2) ratio, 224 [128-297] vs. 332 [187-450]; P < 0.05), and creatinine concentrations increased more in the treated group (from 0.51 [0.42-0.75] to 1.19 [0.64-1.50] mg.dL(-1); P = 0.04) than in the control group (from 0.55 [0.45-0.62] to 0.78 [0.46-1.78] mg.dL(-1); P = 0.12), Enalaprilat therefore prevented the worsening of sublingual microcirculatory variables in this fluid-resuscitated, hyperdynamic model of septic shock, without significant effect on arterial pressure, but with a possible deleterious effect on renal and lung function.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Federal University of Rio de JaneiroUniv Libre Bruxelles, Hop Erasme, Dept Intens Care, B-1070 Brussels, BelgiumUniv Fed Rio de Janeiro, Dept Internal Med, Clementino Fraga Filho Univ Hosp, Rio de Janeiro, BrazilUniv Fed Estado São Paulo, Dept Expt Surg, São Paulo, BrazilAlbert Einstein Hosp, Intens Care Unit, São Paulo, BrazilUniv Fed Estado São Paulo, Dept Expt Surg, São Paulo, BrazilWeb of Science542-549engLippincott Williams & WilkinsShockAngiotensin IIrenal functionsublingual microcirculationSUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCKinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/337232022-09-27 10:00:01.01metadata only accessoai:repositorio.unifesp.br:11600/33723Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-09-27T13:00:01Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK |
title |
SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK |
spellingShingle |
SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK Salgado, Diamantino Ribeiro Angiotensin II renal function sublingual microcirculation |
title_short |
SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK |
title_full |
SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK |
title_fullStr |
SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK |
title_full_unstemmed |
SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK |
title_sort |
SUBLINGUAL MICROCIRCULATORY EFFECTS of ENALAPRILAT in AN OVINE MODEL of SEPTIC SHOCK |
author |
Salgado, Diamantino Ribeiro |
author_facet |
Salgado, Diamantino Ribeiro He, Xinrong Su, Fuhong Sousa, Dalton Barros de Penaccini, Laura Maciel, Leonardo Kfuri Taccone, Fabio Rocco, Jose Rodolfo Silva, Eliezer [UNIFESP] De Backer, Daniel Vincent, Jean-Louis |
author_role |
author |
author2 |
He, Xinrong Su, Fuhong Sousa, Dalton Barros de Penaccini, Laura Maciel, Leonardo Kfuri Taccone, Fabio Rocco, Jose Rodolfo Silva, Eliezer [UNIFESP] De Backer, Daniel Vincent, Jean-Louis |
author2_role |
author author author author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Univ Libre Bruxelles Universidade Federal do Rio de Janeiro (UFRJ) Universidade Federal de São Paulo (UNIFESP) Albert Einstein Hosp |
dc.contributor.author.fl_str_mv |
Salgado, Diamantino Ribeiro He, Xinrong Su, Fuhong Sousa, Dalton Barros de Penaccini, Laura Maciel, Leonardo Kfuri Taccone, Fabio Rocco, Jose Rodolfo Silva, Eliezer [UNIFESP] De Backer, Daniel Vincent, Jean-Louis |
dc.subject.eng.fl_str_mv |
Angiotensin II renal function sublingual microcirculation |
topic |
Angiotensin II renal function sublingual microcirculation |
description |
Severe sepsis is frequently associated with microcirculatory abnormalities despite seemingly adequate hemodynamic resuscitation. As increased serum angiotensin II levels may play a role in this dysfunction, we evaluated the microcirculatory effects of enalaprilat in an experimental model of septic shock. One hour after injection of 1.5 g/kg body weight of feces into the abdominal cavity, 16 adult female anesthetized, mechanically ventilated sheep were randomized to receive 2.5 mg enalaprilat or saline. When fluid-resistant hypotension (mean arterial pressure, <65 mmHg) developed, norepinephrine was given up to a maximal dose of 3 mu g.kg(-1).min(-1). the sublingual microcirculation was evaluated using sidestream dark-field videomicroscopy. A cutoff of 20 mu m was used to differentiate small and large vessels. Experiments were pursued until the sheep's spontaneous death or for a maximum of 30 h. There were progressive and significant reductions in the proportion of small perfused vessels and in the microvascular flow index for small vessels (both P < 0.01 for trend) during shock and the first 2 h of norepinephrine infusion in the placebo group, which were prevented by the administration of enalaprilat. There were no differences between treated and placebo groups in global hemodynamic variables, time to shock or median survival time (21.8 [18.6-28.8] vs. 22.9 [21.8-30.0] h; P = 0.45). However, oxygen exchange was worse (PaO(2)/FIO(2) ratio, 224 [128-297] vs. 332 [187-450]; P < 0.05), and creatinine concentrations increased more in the treated group (from 0.51 [0.42-0.75] to 1.19 [0.64-1.50] mg.dL(-1); P = 0.04) than in the control group (from 0.55 [0.45-0.62] to 0.78 [0.46-1.78] mg.dL(-1); P = 0.12), Enalaprilat therefore prevented the worsening of sublingual microcirculatory variables in this fluid-resuscitated, hyperdynamic model of septic shock, without significant effect on arterial pressure, but with a possible deleterious effect on renal and lung function. |
publishDate |
2011 |
dc.date.issued.fl_str_mv |
2011-06-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:16:47Z |
dc.date.available.fl_str_mv |
2016-01-24T14:16:47Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Shock. Philadelphia: Lippincott Williams & Wilkins, v. 35, n. 6, p. 542-549, 2011. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/33723 http://dx.doi.org/10.1097/SHK.0b013e3182115e6a |
dc.identifier.issn.none.fl_str_mv |
1073-2322 |
dc.identifier.doi.none.fl_str_mv |
10.1097/SHK.0b013e3182115e6a |
dc.identifier.wos.none.fl_str_mv |
WOS:000290662700002 |
identifier_str_mv |
Shock. Philadelphia: Lippincott Williams & Wilkins, v. 35, n. 6, p. 542-549, 2011. 1073-2322 10.1097/SHK.0b013e3182115e6a WOS:000290662700002 |
url |
http://repositorio.unifesp.br/handle/11600/33723 http://dx.doi.org/10.1097/SHK.0b013e3182115e6a |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Shock |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
542-549 |
dc.publisher.none.fl_str_mv |
Lippincott Williams & Wilkins |
publisher.none.fl_str_mv |
Lippincott Williams & Wilkins |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1802764166073679872 |