Open abdomen management treatment of liver injury in rats with abdominal compartment syndrome and sepsis / 中华外科杂志
Chinese Journal of Surgery
;
(12): 335-340, 2011.
Artículo
en Chino
| WPRIM
| ID: wpr-346309
ABSTRACT
<p><b>OBJECTIVE</b>To evaluate the open and closed management treatment of liver injury in rats with sepsis and abdominal compartment syndrome (ACS).</p><p><b>METHODS</b>The sepsis and ACS rats (n = 72) were randomized divided into two groups. One group used closed management (n = 36), the other accepted the open abdomen management (n = 36). The rats were killed at 1, 6 h, 1, 3, 5, 7 d after operation. Blood was collected for liver function tests. Liver sections assessed pathologically and the expressions of Toll-like receptor 4 (TLR4), tumor necrosis factor (TNF)-α, interleukin (IL)-6, signal transducers actuators of transcription (STAT3) and suppressor of cytokine signaling 3 (SOCS3) of rat livers were examined by RT-PCR.</p><p><b>RESULTS</b>The early stage after operation, TNF-α and IL-6 concentrations, STAT3 expressions in rat liver were higher in open abdomen rats than the closed management ones (P < 0.05). TLR4 and SOCS3 expressions were lower in open abdomen rats than the closed management ones (P < 0.05). Aspartate aminotransferase, alanine aminotransferase levels also was lower in open abdomen ones (P < 0.05).</p><p><b>CONCLUSIONS</b>The randomized study demonstrates that open abdomen management could improve liver regeneration in the early stage after operation. Also open abdomen could reduce inflammatory response by reducing TLR4 expressions.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Patología
/
Cirugía General
/
Interleucina-6
/
Factor de Necrosis Tumoral alfa
/
Ratas Sprague-Dawley
/
Sepsis
/
Modelos Animales de Enfermedad
/
Factor de Transcripción STAT3
/
Proteínas Supresoras de la Señalización de Citocinas
/
Receptor Toll-Like 4
Tipo de estudio:
Estudio pronóstico
Límite:
Animales
Idioma:
Chino
Revista:
Chinese Journal of Surgery
Año:
2011
Tipo del documento:
Artículo
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