| Despite advances in supportive care, the mortality rate in patients with acute lung injury (ALI)/acute respiratory distress syndrome still remains high At present, the scholars from home and abroad widely consider the systemic inflammatory response (SIR) plays a key role in the development of ALL/ARDS While in parallel to the inflammatory response, the body mounts a compensatory anti-inflammatory reaction (CAR) in order to counter inflammatory mediators If SIR and CAR are dynamically balanced, homeostasis can be restored So how to enhance CAR and inhibit SIR in order to restore balance and how to interrupt inflammatory cascade reaction have become the focuses of studies on ALI/ ARDS The purpose of our study was designed to investigate the kinetics of inflammatory mediators and anti-inflammatory mediators in the development of ALl, the effects that IL-b or DEX has on inflammatory mediators and anti-inflammatory mediators which may shed light on the mechanism of their protective effects We established a rat model of ALl by intratracheal instillation of LPS with a dose of 1 0mg/kg The 72 SD rats were randomly divided into four groups control group,Endotoxin group~. IL-b + endotoxin group and DEX + endotoxin group, each group included 18 rats which was subdivided into three temporal subgroups (2h, 6h, 24h respectively) We investigated the body weights of rats,artenal gas analyses, the total protein conontration in BALF, the total cell counts and classification in BALF we also determined the concentration of serum TNF- a and BALF TNF- a by RIA RT-PCR method was used to semiquantitatively determine the 3 expression of TNF- a mRNA.. IL-i P mRNA and IL-ira mRNA in lung tissue Furthermore, we examined the lung tissue pathological changes Results: (1) In endotoxin group the body weights of rats severely decreased, Pa 02 dropped progressively, the total protein concentration in BALF increased rapidly 2h after endotoxin administeration and remained high level from then on , the total cells counts increased greatly, Lung pathology showed alveolar srtucture disruption,massive PMN infiltration m lung parenchyma with bleeding and edema (2) In endotoxin group serum TNF- a peaked at 2h, then decreased sharply, while TNF- a in BALF increased rapidly at 2h, peaked at 6h, still higher than control group at 24h (3) In endotoxin group TNF- a mRNA expression in lung tissue peaked at 2h, then decrased sharply, IL-i P mRNA expression greatly mereased at 2h, peaked at 6h,then decreased ,IL-lra mRNA expression peaked at 6h, still higher than control group at 24h (4)IL- 10 and DEX could attenuate body weight losses of rats~. maintain normal Pa 02 .. inhibit the total protein concentration ~. total cells in BALF ... decrease serum TNF- a and TNF- a in BALF, attenuate lung parenchyma injury in pathological examination (5) IL-b and DEX inhibited TNF- a mRNA and IL-i P niRNA expression in lung tissue while had no effect on IL-ira mRNA expression Conclusion: 1 Intratracheal instillation of LPS may serve as a very relevant model to study ARDS 2 Serum inflammatory mediator concentration did not parallel with inflammatory mediator concentration in BALF, the latter may has more sigmficance in assessment of lung injury...
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