Donador exógeno de óxido nítrico en la respuesta inflamatoria hepática y hemodinámica después de choque hemorrágico / Exogenous nitric oxide donor in the liver inflammatory and hemodynamic response after hemorrhagic shock
Cir. & cir
; Cir. & cir;76(4): 291-298, jul.-ago. 2008. graf, ilus
Article
em Es
| LILACS
| ID: lil-568084
Biblioteca responsável:
BR1.1
ABSTRACT
BACKGROUND:
Hemorrhagic shock (HS) results in oxidative stress to cells and in the induction of the inflammatory response, with an increased expression of a number of proinflammatory mediators and cytokines. We tested the ability of the nitric oxide (NO) donor sodium nitroprusside (NP) to reduce tissue injury in a rodent model of uncontrolled hemorrhagic shock.METHODS:
Seventy two Sprague Dawley rats weighing 250-300 g were subjected to a model of uncontrolled hemorrhagic shock. Four groups of animals were included (n = 18 per group) sham/saline, sham/NP, shock/saline, shock/NP. Experimental design consisted of the development of hemorrhagic shock (3 ml/100 g) in a 15-min period, tail amputation (75%) and drug administration at 30 min, fluid resuscitation (FR) with Ringer's lactate (RL) solution to reach a mean arterial pressure (MAP) of 40 mmHg, a hospital phase of 60 min with hemostasis and FR with LR solution to reach a MAP of 70 mmHg, and a 3-day observation phase. Treatment at the beginning of resuscitation included either normal saline (groups 1, 3) or NP (0.5 mg/kg) (groups 2, 4). The following parameters were evaluated fluid requirements for resuscitation, liver injury tests, liver tissue myeloperoxidase (MPO), liver histology, and 3-day survival.RESULTS:
NP significantly reduced fluid requirements for resuscitation (p = 0.0001). We also observed an improved statistically significant difference in tests demonstrating hepatic injury (p = 0.0001), neutrophil infiltration as evidences by liver MPO (p <0.05), and histology studies (p = 0.001). Survival was also increased from 40% in controls to 60% with NP treatment.CONCLUSIONS:
These data suggest that excess NO mediates hemorrhage-induced liver injury, and that the suppression of NO with NP may reduce the pathological consequences of severe hemorrhage, possibly by scavenging superoxide (O(2)(-)), thus limiting the production of more aggressive radicals.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
LILACS
Assunto principal:
Choque Hemorrágico
/
Nitroprussiato
/
Traumatismo por Reperfusão
/
Doadores de Óxido Nítrico
/
Hepatite
/
Circulação Hepática
Limite:
Animals
Idioma:
Es
Revista:
Cir. & cir
Assunto da revista:
CIRURGIA GERAL
Ano de publicação:
2008
Tipo de documento:
Article
País de afiliação:
México
/
Estados Unidos
País de publicação:
México