炎症介质在内毒素引起大鼠肠系膜血管床降钙素基因相关肽释放中的作用

THE ROLE OF INFLAMMATORY MEDIATORS IN ENDOTOXIN INDUCED CGRP RELEASE FROM RAT MESENTERIC ARTERIAL BED

本研究在离体大鼠肠系膜血管床灌流模型上，采用特异放免法测定灌流液中的降钙素基因相关肽（ＣＧＲＰ），观察几种常见炎症介质在内毒素引起ＣＧＲＰ释放中的作用。结果显示：前列腺素合成酶抑制剂地塞米松、布洛芬与消炎痛，缓激肽受体Ｂ２拮抗剂ＨＯＥ１４０，血小板激活因子拮抗剂ＷＥＢ２０８６，组胺Ｈ１受体拮抗剂苯海拉明以及和组胺Ｈ２受体拮抗剂西咪替丁，均能明显抑剂制内毒素引起的ＣＧＲＰ释放，５羟色胺受体拮抗剂ＩＣＳ２０５９３０却无明显作用。从而提示：内毒素引起ＣＧＲＰ释放是通过炎症介质前列腺素、缓激肽、血小板激活因子和组胺介导的，阻断或减少炎症介质的产生可望减轻内毒素血症时ＣＧＲＰ的过量释放。

The role of inflammatorty mediators such as prostaglandins (PGs), bradykinin(BK), platelet activating factor(PAF), histamine and 5 hydroxytryptamine(5 HT)in endotoxin(ETX) induced calcitonin gene related peptide(CGRP) release was studied in isolated rat mesenteric artery bed(MAB). The concentration of CGRP in the perfusate was measured by RIA. The results showed that the CGRP release induced by ETX was inhibited by desamethasone, ibuprofen and indomethasin, all of which are inhibitors of PGs synthetase. HOE 140(BK 2 antagonist), WEB 2086(PAF antagonist), diphenhydramine(histamine H 1 antagonist) and cimetidine(histamine H 2 antagonist)also inhibited the CGRP release induced by ETX, but 5 HT 3 antagonist (ISC205 930) did not show significant effect. The data suggest that PGs, BK, PAF and histamine are involved in the ETX triggered release of CGRP from perivascular nerves in the rat isolated MAB. Blocking the inflammatory mediators might be beneficial in reducing excess release of CGRP during the endotoxicosis.