减阻剂对急性失血性休克合并内毒素致伤二次打击大鼠血清细胞因子水平的影响

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目的观察减阻剂对急性失血性休克合并内毒素致伤二次打击大鼠血清细胞因子水平的影响。方法 60只SD大鼠,雌雄不拘,体质量(331±29)g,随机分为三组,每组20只。在30min内自颈动脉放血完成失血性休克,最终的指标为平均动脉压(40±5)mmHg,然后静脉给予内毒素10mg/kg,休克30min后开始液体复苏。复苏时间为5min,随后继续观察180min。A组为对照组,静脉给予3.5ml/kg的生理盐水;B组使用内含0.4mg/ml的透明质酸和0.05mg/ml聚氧化乙烯作为减阻剂的等量生理盐水复苏;C组复苏液为内含芦荟提取物0.05mg/ml的等量生理盐水。观察大鼠生存情况。在不同时间点测定大鼠血清细胞因子TNF-α、IL-1和IL-10水平的变化。结果 A、B、C三组的生存率分别为20%、60%和65%。A组血清细胞因子TNF-α、IL-1和IL-10浓度均明显增加。与A组相比,减阻剂干预组(B和C组)TNF-α和IL-1水平显著降低(P<0.01),同时IL-10水平明显增加(P<0.01)。但B组和C组各时间点的细胞因子水平无显著性差异(P>0.05)。结论在急性失血性休克复合内毒素二次打击大鼠模型中,减阻剂可提高大鼠生存率,此效果的作用机制之一可能是通过降低促炎性细胞因子TNF-α、IL-1浓度和升高抗炎性细胞因子IL-10水平发挥的。 Objective To observe the effect of anti-dragging agent on the level of serum cytokines in acute hemorrhagic shock combined with endotoxin-induced injury in rats. Methods Sixty male Sprague Dawley rats were randomly divided into three groups (n = 20). The body weight was (331 ± 29) g. Hemorrhagic shock was completed from the carotid arteries in 30 min. The final index was mean arterial pressure (40 ± 5) mmHg, and then the endotoxin was given intravenously at 10 mg / kg. The fluid resuscitation started 30 minutes after shock. Recovery time was 5min, then continue to observe 180min. The rats in group A were given normal saline 3.5ml / kg intravenously. Group B was resuscitated with the same amount of normal saline containing 0.4mg / ml hyaluronic acid and 0.05mg / ml polyethylene oxide as drag reducing agent. Group C Recovery fluid containing aloe extract 0.05mg / ml of equal amount of saline. Observed the survival of rats. The changes of serum cytokines TNF-α, IL-1 and IL-10 in rats at different time points were measured. Results The survival rates of A, B and C groups were 20%, 60% and 65% respectively. A group of serum cytokines TNF-α, IL-1 and IL-10 concentrations were significantly increased. Compared with group A, the levels of TNF-αand IL-1 in DRA-treated group (B and C) were significantly decreased (P <0.01) and IL-10 was significantly increased (P <0.01). However, there was no significant difference in the levels of cytokines between groups B and C at each time point (P> 0.05). Conclusion DRA can increase the survival rate of rats in acute hemorrhagic shock and endotoxin secondary shock model. One of the possible mechanisms may be that the anti-inflammatory cytokines TNF-α and IL-1 Concentration and elevated anti-inflammatory cytokines IL-10 levels play.
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