摘要
作者观察了失血性休克早期大鼠腹腔巨噬细胞分泌ＩＬ－１能力的变化，并初步分析其机制，发现休克后１ｈ、２ｈ巨噬细胞分泌ＩＬ－１的能力分别较失血前提高５１％及６３％，差异均有显著性。此后巨噬细胞分泌ＩＬ－１的能力逐渐降低，至休克后４ｈ较失血前下降３１％，差异有高度显著性。将不同浓度的β－ＥＰ及质皮酮分别与巨噬细胞共同培养，发现前者刺激ＩＬ－１的产生，后者抑制其分泌，均呈量效关系。实验结果提示，在失血早期巨噬细胞分泌ＩＬ－１的能力有显著变化，内源性阿片肽及糖皮质激素可能参与调节失血时巨噬细胞ＩＬ－１的分泌。
The dual phases on secretion of IL-1 by peritoneal macrophages ofhemorrhagic shock rat had been observed. Rats Were shed 30%of their total bloodvolume, and macrophages werc obtained from abdominal cavity of shock rat at varioustime after shed. In the early phase of the shock the macrophage secreting capacity ofIL-1 was increased by 51%and 63%(P<0.05 )at 1h,2h post-shed respectively incomparison with their own baseline value. While it decreased gradually to 31%(P<0.05)of their own baseline value at 4h post-shed. Different dosage ofβ-endorphinand corticosterone were cultured individually with macrophage, it was found thatβ-endorphin stimulated the macrophage secretion of IL-1,while the corticosteroneinhibited it all in dose-dependent manner.These results suggested that macrophage secr-eting capacity of IL-1 changed markedly during the process of hemorrhagic shock,endo-genous opioid peptides and glucocorticoid might mediate IL-1 secreting in macrophage.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1995年第5期512-514,共3页
Chinese Journal of Pathophysiology
