摘要
观察失血性休克早期大鼠、病人IL—1活性变化,大鼠30%失血后,腹腔巨噬细胞分泌IL—1的能力2h内逐渐升高,随后下降,至4h有明显抑制。血浆IL—1活性于2.5h达峰值,随后逐渐下降,无应激大鼠及假处理大鼠IL—1活性均无显著变化。失血性休克患者急诊入院时血浆IL—1活性也显著升高,与健康志愿者相比差异显著,其机制及意义有待探讨。
The in vivo and in vitro changes of IL-1 activity in the early phase of hemorrhagic shock of rats and patient were observed. Experimental hemorrhagic shock model was produced by exsanguinate 30% of rats total blood volume. Hemorrhagic shock patient was affirmed according to bloodloss history and brachial artery pressure. IL - 1 activity was detected by improved lymphocyte-activating factor (LAF) method. It was found that there was an initial increase and followed by a decrease in plasma IL-1 activity as well as IL-1 secreting capacity of peritoneal macrophage in the intial 4 hours of shock. However there was no obvious change of IL -1 activity in nonstress or sham rat. Shock patients just like shock rats also exhibited an enhanced plasma IL-1 activity at time of admission, but the volunteer did not. The mechanism and meaning of IL-1 alteration in hemorrhagic shock is worth further study.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1997年第3期317-320,共4页
Chinese Journal of Pathophysiology