| Texto completo | |
| Autor(es): Mostrar menos - |
Moretti, Eduardo H.
;
Rodrigues, Abner C.
;
Marques, Bruno V.
;
Totola, Leonardo T.
;
Ferreira, Caroline B.
;
Brito, Camila F.
;
Matos, Caroline M.
;
da Silva, Filipe A.
;
Santos, Robson A. S.
;
Lopes, Luciana B.
;
Moreira, Thiago S.
;
Akamine, Eliana H.
;
Baccala, Luiz A.
;
Fujita, Andre
;
Steiner, Alexandre A.
Número total de Autores: 15
|
| Tipo de documento: | Artigo Científico |
| Fonte: | PNAS NEXUS; v. 2, n. 2, p. 13-pg., 2023-02-01. |
| Resumo | |
Uncontrolled vasodilation is known to account for hypotension in the advanced stages of sepsis and other systemic inflammatory conditions, but the mechanisms of hypotension in earlier stages of such conditions are not clear. By monitoring hemodynamics with the highest temporal resolution in unanesthetized rats, in combination with ex-vivo assessment of vascular function, we found that early development of hypotension following injection of bacterial lipopolysaccharide is brought about by a fall in vascular resistance when arterioles are still fully responsive to vasoactive agents. This approach further uncovered that the early development of hypotension stabilized blood flow. We thus hypothesized that prioritization of the local mechanisms of blood flow regulation (tissue autoregulation) over the brain-driven mechanisms of pressure regulation (baroreflex) underscored the early development of hypotension in this model. Consistent with this hypothesis, an assessment of squared coherence and partial-directed coherence revealed that, at the onset of hypotension, the flow-pressure relationship was strengthened at frequencies (<0.2 Hz) known to be associated with autoregulation. The autoregulatory escape to phenylephrine-induced vasoconstriction, another proxy of autoregulation, was also strengthened in this phase. The competitive demand that drives prioritization of flow over pressure regulation could be edema-associated hypovolemia, as this became detectable at the onset of hypotension. Accordingly, blood transfusion aimed at preventing hypovolemia brought the autoregulation proxies back to normal and prevented the fall in vascular resistance. This novel hypothesis opens a new avenue of investigation into the mechanisms that can drive hypotension in systemic inflammation. (AU) | |
| Processo FAPESP: | 18/13877-1 - Nanocarreadores para a quimioprevenção e tratamento localizado de tumores de mama |
| Beneficiário: | Luciana Biagini Lopes |
| Modalidade de apoio: | Auxílio à Pesquisa - Jovens Pesquisadores - Fase 2 |
| Processo FAPESP: | 20/00631-4 - Desenvolvimento de hipotermia na inflamação sistêmica: a hipótese da sinalização criogênica |
| Beneficiário: | Caroline Martins de Matos |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado Direto |
| Processo FAPESP: | 18/03418-0 - Hipotermia na Sepse: causas e consequências |
| Beneficiário: | Alexandre Alarcon Steiner |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 20/09399-7 - Desenvolvimento de hipotermia na inflamação sistêmica: a hipótese da hipóxia encefálica. |
| Beneficiário: | Eduardo Hermogenes Moretti |
| Modalidade de apoio: | Bolsas no Brasil - Pós-Doutorado |
| Processo FAPESP: | 15/23376-1 - Núcleo retrotrapezóide, quimiossensibilidade central e automaticidade respiratória |
| Beneficiário: | Thiago dos Santos Moreira |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 18/21934-5 - Estatística de redes: teoria, métodos e aplicações |
| Beneficiário: | André Fujita |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |