Platelet-derived exosomes from septic shock patients induce myocardial dysfunction
Autor(a) principal: | |
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Data de Publicação: | 2007 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1186/cc6176 http://repositorio.unifesp.br/handle/11600/29345 |
Resumo: | Introduction Mechanisms underlying inotropic failure in septic shock are incompletely understood. We previously identified the presence of exosomes in the plasma of septic shock patients. These exosomes are released mainly by platelets, produce superoxide, and induce apoptosis in vascular cells by a redox-dependent pathway. We hypothesized that circulating platelet-derived exosomes could contribute to inotropic dysfunction of sepsis.Methods We collected blood samples from 55 patients with septic shock and 12 healthy volunteers for exosome separation. Exosomes from septic patients and healthy individuals were investigated concerning their myocardial depressant effect in isolated heart and papillary muscle preparations.Results Exosomes from the plasma of septic patients significantly decreased positive and negative derivatives of left ventricular pressure in isolated rabbit hearts or developed tension and its first positive derivative in papillary muscles. Exosomes from healthy individuals decreased these variables non-significantly. in hearts from rabbits previously exposed to endotoxin, septic exosomes decreased positive and negative derivatives of ventricular pressure. This negative inotropic effect was fully reversible upon withdrawal of exosomes. Nitric oxide ( NO) production from exosomes derived from septic shock patients was demonstrated by fluorescence. Also, there was an increase in myocardial nitrate content after exposure to septic exosomes.Conclusion Circulating platelet-derived exosomes from septic patients induced myocardial dysfunction in isolated heart and papillary muscle preparations, a phenomenon enhanced by previous in vivo exposure to lipopolysaccharide. the generation of NO by septic exosomes and the increased myocardial nitrate content after incubation with exosomes from septic patients suggest an NO-dependent mechanism that may contribute to myocardial dysfunction of sepsis. |
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Repositório Institucional da UNIFESP |
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3465 |
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Platelet-derived exosomes from septic shock patients induce myocardial dysfunctionIntroduction Mechanisms underlying inotropic failure in septic shock are incompletely understood. We previously identified the presence of exosomes in the plasma of septic shock patients. These exosomes are released mainly by platelets, produce superoxide, and induce apoptosis in vascular cells by a redox-dependent pathway. We hypothesized that circulating platelet-derived exosomes could contribute to inotropic dysfunction of sepsis.Methods We collected blood samples from 55 patients with septic shock and 12 healthy volunteers for exosome separation. Exosomes from septic patients and healthy individuals were investigated concerning their myocardial depressant effect in isolated heart and papillary muscle preparations.Results Exosomes from the plasma of septic patients significantly decreased positive and negative derivatives of left ventricular pressure in isolated rabbit hearts or developed tension and its first positive derivative in papillary muscles. Exosomes from healthy individuals decreased these variables non-significantly. in hearts from rabbits previously exposed to endotoxin, septic exosomes decreased positive and negative derivatives of ventricular pressure. This negative inotropic effect was fully reversible upon withdrawal of exosomes. Nitric oxide ( NO) production from exosomes derived from septic shock patients was demonstrated by fluorescence. Also, there was an increase in myocardial nitrate content after exposure to septic exosomes.Conclusion Circulating platelet-derived exosomes from septic patients induced myocardial dysfunction in isolated heart and papillary muscle preparations, a phenomenon enhanced by previous in vivo exposure to lipopolysaccharide. the generation of NO by septic exosomes and the increased myocardial nitrate content after incubation with exosomes from septic patients suggest an NO-dependent mechanism that may contribute to myocardial dysfunction of sepsis.Univ São Paulo, Sch Med, Emergency Med Res Lab, BR-05403900 São Paulo, BrazilHosp Sirio Libanes, Res & Educ Inst, BR-01308060 São Paulo, BrazilUniv São Paulo, Inst Biomed Sci, Dept Pharm, BR-05508900 São Paulo, BrazilUniv São Paulo, Heart Inst InCor, Vasc Biol Lab, BR-05403000 São Paulo, BrazilUniversidade Federal de São Paulo, Cardiovasc Physiol Lab, BR-04022000 São Paulo, BrazilUniversidade Federal de São Paulo, Cardiovasc Physiol Lab, BR-04022000 São Paulo, BrazilWeb of ScienceBiomed Central LtdUniversidade de São Paulo (USP)Hosp Sirio LibanesUniversidade Federal de São Paulo (UNIFESP)Azevedo, Luciano Cesar PontesJaniszewski, MarianoPontieri, VeraPedro, Marcelo de AlmeidaBassi, EstevaoTucci, Paulo Jose Ferreira [UNIFESP]Laurindo, Francisco Rafael Martins2016-01-24T12:41:42Z2016-01-24T12:41:42Z2007-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion10application/pdfhttp://dx.doi.org/10.1186/cc6176Critical Care. London: Biomed Central Ltd, v. 11, n. 6, 10 p., 2007.10.1186/cc6176WOS000253286500004.pdf1466-609Xhttp://repositorio.unifesp.br/handle/11600/29345WOS:000253286500004engCritical Careinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-08-07T14:12:08Zoai:repositorio.unifesp.br/:11600/29345Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-08-07T14:12:08Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Platelet-derived exosomes from septic shock patients induce myocardial dysfunction |
title |
Platelet-derived exosomes from septic shock patients induce myocardial dysfunction |
spellingShingle |
Platelet-derived exosomes from septic shock patients induce myocardial dysfunction Azevedo, Luciano Cesar Pontes |
title_short |
Platelet-derived exosomes from septic shock patients induce myocardial dysfunction |
title_full |
Platelet-derived exosomes from septic shock patients induce myocardial dysfunction |
title_fullStr |
Platelet-derived exosomes from septic shock patients induce myocardial dysfunction |
title_full_unstemmed |
Platelet-derived exosomes from septic shock patients induce myocardial dysfunction |
title_sort |
Platelet-derived exosomes from septic shock patients induce myocardial dysfunction |
author |
Azevedo, Luciano Cesar Pontes |
author_facet |
Azevedo, Luciano Cesar Pontes Janiszewski, Mariano Pontieri, Vera Pedro, Marcelo de Almeida Bassi, Estevao Tucci, Paulo Jose Ferreira [UNIFESP] Laurindo, Francisco Rafael Martins |
author_role |
author |
author2 |
Janiszewski, Mariano Pontieri, Vera Pedro, Marcelo de Almeida Bassi, Estevao Tucci, Paulo Jose Ferreira [UNIFESP] Laurindo, Francisco Rafael Martins |
author2_role |
author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade de São Paulo (USP) Hosp Sirio Libanes Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Azevedo, Luciano Cesar Pontes Janiszewski, Mariano Pontieri, Vera Pedro, Marcelo de Almeida Bassi, Estevao Tucci, Paulo Jose Ferreira [UNIFESP] Laurindo, Francisco Rafael Martins |
description |
Introduction Mechanisms underlying inotropic failure in septic shock are incompletely understood. We previously identified the presence of exosomes in the plasma of septic shock patients. These exosomes are released mainly by platelets, produce superoxide, and induce apoptosis in vascular cells by a redox-dependent pathway. We hypothesized that circulating platelet-derived exosomes could contribute to inotropic dysfunction of sepsis.Methods We collected blood samples from 55 patients with septic shock and 12 healthy volunteers for exosome separation. Exosomes from septic patients and healthy individuals were investigated concerning their myocardial depressant effect in isolated heart and papillary muscle preparations.Results Exosomes from the plasma of septic patients significantly decreased positive and negative derivatives of left ventricular pressure in isolated rabbit hearts or developed tension and its first positive derivative in papillary muscles. Exosomes from healthy individuals decreased these variables non-significantly. in hearts from rabbits previously exposed to endotoxin, septic exosomes decreased positive and negative derivatives of ventricular pressure. This negative inotropic effect was fully reversible upon withdrawal of exosomes. Nitric oxide ( NO) production from exosomes derived from septic shock patients was demonstrated by fluorescence. Also, there was an increase in myocardial nitrate content after exposure to septic exosomes.Conclusion Circulating platelet-derived exosomes from septic patients induced myocardial dysfunction in isolated heart and papillary muscle preparations, a phenomenon enhanced by previous in vivo exposure to lipopolysaccharide. the generation of NO by septic exosomes and the increased myocardial nitrate content after incubation with exosomes from septic patients suggest an NO-dependent mechanism that may contribute to myocardial dysfunction of sepsis. |
publishDate |
2007 |
dc.date.none.fl_str_mv |
2007-01-01 2016-01-24T12:41:42Z 2016-01-24T12:41:42Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1186/cc6176 Critical Care. London: Biomed Central Ltd, v. 11, n. 6, 10 p., 2007. 10.1186/cc6176 WOS000253286500004.pdf 1466-609X http://repositorio.unifesp.br/handle/11600/29345 WOS:000253286500004 |
url |
http://dx.doi.org/10.1186/cc6176 http://repositorio.unifesp.br/handle/11600/29345 |
identifier_str_mv |
Critical Care. London: Biomed Central Ltd, v. 11, n. 6, 10 p., 2007. 10.1186/cc6176 WOS000253286500004.pdf 1466-609X WOS:000253286500004 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Critical Care |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
10 application/pdf |
dc.publisher.none.fl_str_mv |
Biomed Central Ltd |
publisher.none.fl_str_mv |
Biomed Central Ltd |
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 |
biblioteca.csp@unifesp.br |
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1814268299526012928 |