Role of LPS in the hepatic microvascular dysfunction elicited by cecal ligation and puncture in mice.
J Hepatol
; 47(6): 799-806, 2007 Dec.
Article
em En
| MEDLINE
| ID: mdl-17935822
ABSTRACT
BACKGROUND/AIMS:
Sepsis remains a leading cause of death in critically ill patients. Because endotoxemia is viewed as a key mediator of sepsis-induced inflammation, administration of bacterial endotoxin (LPS) is often used to simulate sepsis in experimental animals. This study tests the hypothesis that LPS is a critical determinant of the hepatic microvascular dysfunction in mice made septic by cecal ligation and puncture (CLP).METHODS:
Intravital videomicroscopy was used to quantify sinusoidal perfusion, and platelet and leukocyte adhesion in terminal hepatic venules (THV) and sinusoids in LPS-sensitive and LPS-insensitive mice subjected to CLP or LPS (i.p.). mRNA expression of TLR-2, TLR-4, MyD-88, and Ly-96 was also assessed.RESULTS:
While LPS-sensitive mice responded to both CLP and LPS challenges with elevated leukocyte and platelet adhesion in THV and sinusoids, and a reduced sinusoidal perfusion density, LPS-insensitive mice exhibited comparable blood cell adhesion and sinusoidal malperfusion following CLP, but not LPS. Hepatic mRNA of MyD-88 and TLR-2 was elevated in the CLP and LPS groups. Endotoxin was not detectable in the blood of LPS-sensitive mice after CLP, but was elevated after LPS administration.CONCLUSIONS:
These findings do not support a major role for LPS in the hepatic microvascular disturbances associated with polymicrobial sepsis.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Lipopolissacarídeos
/
Sepse
/
Circulação Hepática
/
Hepatopatias
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article
País de afiliação:
Áustria