Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats

Detalhes bibliográficos
Autor(a) principal: Simas, Rafael
Data de Publicação: 2015
Outros Autores: Ferreira, Sueli G., Menegat, Laura, Zanoni, Fernando L., Correia, Cristiano J., Silva, Isaac A., Sannomiya, Paulina, Moreira, Luiz F.P.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/101078
Resumo: OBJECTIVES: Brain death is typically followed by autonomic changes that lead to hemodynamic instability, which is likely associated with microcirculatory dysfunction and inflammation. We evaluated the role of the microcirculation in the hemodynamic and inflammatory events that occur after brain death and the effects of autonomic storm inhibition via thoracic epidural blockade on mesenteric microcirculatory changes and inflammatory responses. METHODS: Male Wistar rats were anesthetized and mechanically ventilated. Brain death was induced via intracranial balloon inflation. Bupivacaine (brain death-thoracic epidural blockade group) or saline (brain death group) infusion via an epidural catheter was initiated immediately before brain death induction. Sham-operated animals were used as controls (SH group). The mesenteric microcirculation was analyzed via intravital microscopy, and the expression of adhesion molecules was evaluated via immunohistochemistry 180 min after brain death induction. RESULTS: A significant difference in mean arterial pressure behavior was observed between the brain death-thoracic epidural blockade group and the other groups, indicating that the former group experienced autonomic storm inhibition. However, the proportion of perfused small vessels in the brain death-thoracic epidural blockade group was similar to or lower than that in the brain death and SH groups, respectively. The expression of intercellular adhesion molecule 1 was similar between the brain death-thoracic epidural blockade and brain death groups but was significantly lower in the SH group than in the other two groups. The number of migrating leukocytes in the perivascular tissue followed the same trend for all groups. CONCLUSIONS: Although thoracic epidural blockade effectively inhibited the autonomic storm, it did not affect mesenteric hypoperfusion or inflammation induced by brain death.
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spelling Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats OBJECTIVES: Brain death is typically followed by autonomic changes that lead to hemodynamic instability, which is likely associated with microcirculatory dysfunction and inflammation. We evaluated the role of the microcirculation in the hemodynamic and inflammatory events that occur after brain death and the effects of autonomic storm inhibition via thoracic epidural blockade on mesenteric microcirculatory changes and inflammatory responses. METHODS: Male Wistar rats were anesthetized and mechanically ventilated. Brain death was induced via intracranial balloon inflation. Bupivacaine (brain death-thoracic epidural blockade group) or saline (brain death group) infusion via an epidural catheter was initiated immediately before brain death induction. Sham-operated animals were used as controls (SH group). The mesenteric microcirculation was analyzed via intravital microscopy, and the expression of adhesion molecules was evaluated via immunohistochemistry 180 min after brain death induction. RESULTS: A significant difference in mean arterial pressure behavior was observed between the brain death-thoracic epidural blockade group and the other groups, indicating that the former group experienced autonomic storm inhibition. However, the proportion of perfused small vessels in the brain death-thoracic epidural blockade group was similar to or lower than that in the brain death and SH groups, respectively. The expression of intercellular adhesion molecule 1 was similar between the brain death-thoracic epidural blockade and brain death groups but was significantly lower in the SH group than in the other two groups. The number of migrating leukocytes in the perivascular tissue followed the same trend for all groups. CONCLUSIONS: Although thoracic epidural blockade effectively inhibited the autonomic storm, it did not affect mesenteric hypoperfusion or inflammation induced by brain death. Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2015-06-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/10107810.6061/clinics/2015(06)11Clinics; Vol. 70 No. 6 (2015); 446-452Clinics; v. 70 n. 6 (2015); 446-452Clinics; Vol. 70 Núm. 6 (2015); 446-4521980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/101078/99737Copyright (c) 2015 Clinicsinfo:eu-repo/semantics/openAccessSimas, Rafael Ferreira, Sueli G. Menegat, Laura Zanoni, Fernando L. Correia, Cristiano J. Silva, Isaac A. Sannomiya, Paulina Moreira, Luiz F.P. 2015-07-28T15:24:29Zoai:revistas.usp.br:article/101078Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2015-07-28T15:24:29Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
title Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
spellingShingle Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
Simas, Rafael
title_short Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
title_full Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
title_fullStr Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
title_full_unstemmed Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
title_sort Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
author Simas, Rafael
author_facet Simas, Rafael
Ferreira, Sueli G.
Menegat, Laura
Zanoni, Fernando L.
Correia, Cristiano J.
Silva, Isaac A.
Sannomiya, Paulina
Moreira, Luiz F.P.
author_role author
author2 Ferreira, Sueli G.
Menegat, Laura
Zanoni, Fernando L.
Correia, Cristiano J.
Silva, Isaac A.
Sannomiya, Paulina
Moreira, Luiz F.P.
author2_role author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Simas, Rafael
Ferreira, Sueli G.
Menegat, Laura
Zanoni, Fernando L.
Correia, Cristiano J.
Silva, Isaac A.
Sannomiya, Paulina
Moreira, Luiz F.P.
description OBJECTIVES: Brain death is typically followed by autonomic changes that lead to hemodynamic instability, which is likely associated with microcirculatory dysfunction and inflammation. We evaluated the role of the microcirculation in the hemodynamic and inflammatory events that occur after brain death and the effects of autonomic storm inhibition via thoracic epidural blockade on mesenteric microcirculatory changes and inflammatory responses. METHODS: Male Wistar rats were anesthetized and mechanically ventilated. Brain death was induced via intracranial balloon inflation. Bupivacaine (brain death-thoracic epidural blockade group) or saline (brain death group) infusion via an epidural catheter was initiated immediately before brain death induction. Sham-operated animals were used as controls (SH group). The mesenteric microcirculation was analyzed via intravital microscopy, and the expression of adhesion molecules was evaluated via immunohistochemistry 180 min after brain death induction. RESULTS: A significant difference in mean arterial pressure behavior was observed between the brain death-thoracic epidural blockade group and the other groups, indicating that the former group experienced autonomic storm inhibition. However, the proportion of perfused small vessels in the brain death-thoracic epidural blockade group was similar to or lower than that in the brain death and SH groups, respectively. The expression of intercellular adhesion molecule 1 was similar between the brain death-thoracic epidural blockade and brain death groups but was significantly lower in the SH group than in the other two groups. The number of migrating leukocytes in the perivascular tissue followed the same trend for all groups. CONCLUSIONS: Although thoracic epidural blockade effectively inhibited the autonomic storm, it did not affect mesenteric hypoperfusion or inflammation induced by brain death.
publishDate 2015
dc.date.none.fl_str_mv 2015-06-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/101078
10.6061/clinics/2015(06)11
url https://www.revistas.usp.br/clinics/article/view/101078
identifier_str_mv 10.6061/clinics/2015(06)11
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/101078/99737
dc.rights.driver.fl_str_mv Copyright (c) 2015 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2015 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 70 No. 6 (2015); 446-452
Clinics; v. 70 n. 6 (2015); 446-452
Clinics; Vol. 70 Núm. 6 (2015); 446-452
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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