rhEDIL—8抗大鼠失血性休克的实验研究

AN EXPERIMETAL STUDY ON ANTI—HEMORRHAGIC SHOCK EFFECT OF rhEDIL—8 IN RATS

Wistar大鼠32只,股动脉放血复制晚期失血性休克模型(MABP,5.3kPa;维持90 min),给予rhEDIL—8250μg·kg^(-1)i.v。结果表明,晚期失血性休克单纯输血补液其MABP 为一过性升高,输血补液后30min 即见MABP 明显降低,2hrMABP 为5kPa,相当于原血压的32.84%,动物仍处于休克状态。给予rbEDIL—8后,MABP 明显升高,2hrMABP 为9.4kPa,相当于原血压的60.62%休克状态明显改善,2hr 存活率显著提高。IL—8的抗休克作用可能与其抑制内皮收缩因子(EDCF)的释放、促进内皮舒张因子(EDRF)的释放有关。从而起到扩张血管、改善组织灌流的作用。因为假休克组提示:单纯给予IL—8有扩张血管降压作用。

The effect of recombinant human endothelium-derived Interleulin-8(rhEDIL—8)on hemorrhagic shock in rats was studied.A profound hemorrh-agic shock(mean arterial blood pressure,5.3kPa)model was produced inrats by bleeding from femoral artery into a reservoir and maintained at MABP5.3kPa by further bleeding or auto-transfusion for 90 min.After that all theblood shed outside and then the normal saline(15ml/Kg)were transfused i.v.rhEDIL-8 250ug/kg was given to the sham and shock groups.the resultsshowed that the MABP of the shock control group lowered signi ficantly afterbeing shortly raised.After administration of rhEDIL-8,the MABP of theanimals of shock treated group elevated obviously,shock condition was improvedmarkedly and the survivaI rate at 2 hr after reinfusion was increased.In thesham shock group,contrary,admlnistration of rhEDIL-8 caused hypotesion.Itsuggests that rhEDIL-8 dilates the vasculature through inhibiting release ofendothelium-derived contracting factor and promoting release of endothelium-de-rived relaxng factor That may be its mechanism of anti-shock effects.