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https://www.arca.fiocruz.br/handle/icict/32293
Tipo de documento
ArtigoDireito Autoral
Acesso aberto
Data de embargo
2020-03-01
Coleções
- INI - Artigos de Periódicos [3392]
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CEREBRAL MULTIMODAL MONITORING IN SEPSIS: AN EXPERIMENTAL STUDY
Cerebral multimodality monitoring
Sepsis-associated encephalopathy
Autor(es)
Afiliação
Paulo Niemeyer State Brain Institute. Rio de Janeiro, RJ, Brazil.
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Fundação Oswaldo Cruz. Instituto Nacional de Infectologia. Rio de Janeiro, RJ, Brasil / Instituto D’Or de Ensino e Pesquisa. Rio de Janeiro, RJ, Brasil.
Sem afiliação.
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Sem afiliação.
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Fundação Oswaldo Cruz. Instituto Nacional de Infectologia. Rio de Janeiro, RJ, Brasil / Instituto D’Or de Ensino e Pesquisa. Rio de Janeiro, RJ, Brasil.
Resumo em Inglês
Acute brain dysfunction is a complication of sepsis, and its pathophysiology remains poorly understood. We
studied the brain metabolism in a resuscitated animal model of sepsis. Twelve anesthetized, mechanically ventilated, and invasively monitored pigs were allocated to a sham procedure (N ¼ 5) or sepsis (N ¼ 7). Sepsis was induced through fecal inoculation in the peritoneum. Fluid resuscitation was maintained during the entire study period. Animals were observed until spontaneous death or for a maximum of 24 h. In addition to global hemodynamic and laboratory assessment, intracranial pressure and cerebral microdialysis (MD) were evaluated at baseline, 6, 12, 18, and 24 h after sepsis induction. After euthanasia, the brain was rapidly removed and a fragment from the frontal cortex was analyzed for markers of neuroinflammation, metabolism, and neurotransmission. Septic animals developed a hyperdynamic state associated with increased arterial lactate. Cerebral microdialysis showed unchanged levels of lactate/pyruvate ratios and brain glucose between the groups. Brain/serum glucose ratios were increased in the septic animals during the study period despite a progressive decrease in serum glucose. Moreover, extracellular glutamine levels were elevated starting at 6 h after sepsis. Tissue analysis showed elevated glutamate, glutamine, and glutamine synthetase in the sepsis group. However, C-Fos, a marker of neuronal activity, was unchanged between groups. In this animal model of resuscitated sepsis, we found increased oxidative stress and alterations in neuroenergetics characterized by exacerbated activity of the glutamate/glutamine cycle and increased glucose utilization by the brain, however without any evidence of decompensated energy metabolism.
Palavras-chave em inglês
Acute brain dysfunctionCerebral multimodality monitoring
Sepsis-associated encephalopathy
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