THE EFFECTS OF ESCHARECTOMY DURING BURN SHOCK STAGE ON THE mRNA EXPRESSION OF INTERCELLULAR ADHESION MOLECULE-1 AND TUMOR NECROSIS FACTOR-? IN RAT LIVER
- VernacularTitle:休克期切痂对大鼠肝组织ICAM-1及TNF-? mRNA表达的影响
- Author:
Lixin HE
;
Zhenrong GUO
;
Jiak CHAI
- Publication Type:Journal Article
- Keywords:
Burns;
escharectomy;
adhesion molecules;
RT PCR
- From:
Medical Journal of Chinese People's Liberation Army
2001;0(07):-
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the changes in the expression of intercellular adhesion molecule 1(ICAM 1) ,tumor necrosis factor ?(TNF ?) mRNA and MPO activity in rat liver after burns and the effects of escharectomy during burn shock stage on the expression of these parameters. One hundred and seventy six Wistar rats with 30% TBSA full thickness thermal injury were used. The mRNA expression of ICAM 1 and TNF ? were detected by reverse transcription polymerase chain reaction(RT PCR) in liver tissues at various intervals after burns with or without escharectomy during shock stage. Both expression of ICAM 1 and TNF ?mRNA in rat liver after burns began to increase at 4h postburn and peaked at 12h and 24h, respectively. Afterwards in groups of escharectomy at 8h and 24h postburn, the expressions of both ICAM 1 and TNF ? increased again, though the expression values were lower than the first peak values, and they returned to normal range at 96h postburn. But in groups of burn control and escharectomy at 96h postburn, their expressions still remained high on 7d postburn. In addition, MPO activity returned to normal levels at 96h postburn in groups with escharectomy during shock stage, while in groups burn control and escharectomy at 96h postburn, a high value of MPO activity persisted till 7d postburn. Our findings suggest that eschar could induce the production of inflammatory mediators such as ICAM 1 and TNF ? which damaged endothelial cells. Therefore, escharectomy as early as possible may play an important role in preventing the expression and release of adhesion molecules and the development of systemsc lnflammatory response syndrome.
