醋酸奥曲肽对兔肝缺血再灌注损伤内毒素及炎性细胞因子的影响

目的 观察醋酸奥曲肽对兔肝脏缺血再灌注损伤后内毒素及炎性细胞因子的影响.方法 采用Pringle's兔肝脏缺血再灌注模型,将24只新西兰大白兔随机分为3组:假手术组(A组)、肝脏缺血再灌注组(B组)和醋酸奥曲肽预适应组(C组).观察三组动物肝门阻断前(T1)、阻断后30 min(T2)、再灌注30 min(T3)、再灌注120 min(T4)各时点血浆内毒素(ETX)及血清肿瘤坏死因子α(TNF-α)、白介素-1β(IL-1β)的变化.结果 B、C组从T2开始内毒素(ETX)与A组比较明显升高(P<0.05),且C组明显低于B组(P<0.05);B组从T2开始、C组从T3开始TNF-α明显高于A组(P<0.05),C组从T2开始TNF-α明显低于B组(P<0.05);B组、C组从T2开始IL-1β明显高于A组(P<0.05),且C组又明显低于B组(P<0.05).结论 醋酸奥曲肽可以降低肝脏缺血再灌损伤兔血浆中内毒素水平及下调血清TNF-α、IL-1β等炎症介质,这可能是它对兔肝脏缺血再灌注损伤保护作用的机制之一.

The effect of octreotide acetate on plasma ETX and serum inflammatory cytokine of the rabbit with hepatic Ischemia-reperfusion Injury

Objective To observe the effect of octreotide acetate on plasma ETX and serum inflammatory cytokine of the rabbit with hepatic ischcmia reperfusion injury. Methods Pringle's maneuver rabbit hepatic ischemia-repeffusion models were established. 24 adult New Zealand rabbits were random divided into equal 3 groups: sham operative group(group A), iacbemia reperfusion group(group B)and octreotide acetate preconditioning group(group C). Endotoxin (ETX) in the plasma, tumor necrosis factor-alpha (TNF-α) and intcdeukin-1beta (IL-1β) were detected in every rabbit at the time before iachemia (T1), 30min after ischemia (T2), 30min (T3) and 120min (T4) after reperfusion. Results From T2 to T4, the ETX in group B and C were higher than that in group A (P < 0.05), the ETX of group C were lower than that in group B (P<0.05). From T2 to T4, the TNF-α of group B and C were higher than that of group A(P<0.05). From T3 to T4 the TNF-α of group C were higher than that of group A(P<0.05). From T2 to T4,the IL-1β of group B and group C were higher than that of group A(P<0.05), and the IL-1β of group C were lower than that of group B (P<0.05). Conclusion Octreotide acetate can decrease plasma ETX and down-regulate inflammation factors, such as TNFαand IL-1β, in serum of the rabbit with hepatic iacbe-mia-reperfusion injury, which may be the protective mechanism of oetreotide acetate on rabbit hepatic isehemia-reperfusiun injury.