Inhibition of complement C3 might rescue vascular hyporeactivity in a conscious hemorrhagic shock rat model.
Microvasc Res
; 105: 23-9, 2016 May.
Article
em En
| MEDLINE
| ID: mdl-26687560
ABSTRACT
BACKGROUND:
Vascular hyporeactivity in severe hemorrhagic shock could induce refractory hypotension and is an important cause of death. The global acute inflammatory response induced in shock triggers the over-expression of reactive oxygen species, NO, ET1 and TNF-α, which play essential roles in the pathology of vascular hyporeactivity. This leads to a hypothesis that inhibition of the complement system, the mediator of the inflammatory cascade, might be a promising therapeutic exploration for vascular hyporeactivity.METHODS:
We use cobra venom factor (CVF) and the soluble form of CR1 (sCR1) which deplete or inhibit complement C3 respectively to examine its role in vascular hyporeactivity in a conscious hemorrhagic shock rat model.RESULTS:
We first confirmed the over-activation of C3 during shock and the down-regulation effects of CVF and sCR1 on C3. Then, both CVF and sCR1 could significantly mitigate the over-expression of serum NO, ET-1, TNF-α and reactive oxygen species. Finally, the vascular reactivity of superior mesenteric arteries (SMA) was examined in vitro, which confirmed the massive reduction of vascular reactivity in shock, which was significantly rescued by both CVF and sCR1.CONCLUSIONS:
Inhibition of C3 might improve the reactivity of SMA to norepinephrine during hemorrhagic shock possibly through the downregulation of NO, ET1, TNF-α and reactive oxygen radicals.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Choque Hemorrágico
/
Vasoconstrição
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Vasoconstritores
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Complemento C3
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Receptores de Complemento 3b
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Artéria Mesentérica Superior
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Ativação do Complemento
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Venenos Elapídicos
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Inativadores do Complemento
Tipo de estudo:
Etiology_studies
/
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Microvasc Res
Ano de publicação:
2016
Tipo de documento:
Article