白细胞介素—8的抗休克机制研究

STUDIES ON MECHANISM OF ANTI-SHOCK EFFECT OF INTERLEUKIN-8 IN RATS

为探讨ＩＬ—８的抗休克机制，本实验应用ＰｅｎｉｎｓｕｌａＬａｂ放免药盒测定大鼠失血性休克前后及给予ｒｈＥＤＩＬ—８后血浆ＥＴ水平。结果表明：晚期失血性休克血浆ＥＴ明显升高（２１．３５±４．１３ｐｇ／ｍｌ，正常８．２３±１．７６Ｐｇ／ｍｌ），给予ｒｈＥＤＩＬ—８２５０μｇ／ｋｇ后ｈ２，血浆ＥＴ明显降低（９．６４±３．８４ｐｇ／ｍｌ），休克状态明显改善，与休克对照组相比有高度显著性差异（ｐ＜０．０１）。ＩＬ—８对假休克大鼠的降压作用与ＥＴ无明显关系。提示：ＩＬ—８具有抑制内皮细胞ＥＴ的异常分泌，从而恢复和保护血管的正常反应性调节，可能是其抗休克的重要机制。

In order to investigate the mechanism of antishock effect of interleukin- 8, plasma endothelin-I concentrations. (before shock, after shock, and after administration of rhEDIL-8) were measured by the methdo of radimmunoassay. The results showed that plasma endothelin- I level was markedly increased during advanced hemorrhagic shock (21.35±4 /13 pg/ml against normal 8.23±1.76pg/ml). After administration of rhEDIL- 8, the plasma endothelin -I level was obviously lowered (9.64±3.84pg/ml), and the,shock condition was remarkab ly improved. Compared with the shock control group, the difference was quite significant (P<0 .01 ). Hypotension caused by IL-- 8 in the sham shock had nothing to do with endothelin-I. The results suggest that interleukin-- 8 in hibits alnormal secretion of endothein-I in endothelium and preserves the vasoactive regulation of the shocked animal. That may be its mechanism of anti-shock effect.