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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ＨＯＥ１４０，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ＩＣＳ２０５９３０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。
In this study, we used specific radioimmunoassay to detect calcitonin gene-related peptide (CGRP) in the rat mesenteric vascular bed perfusion model and observed the role of several common inflammatory mediators in endotoxin-induced CGRP release. The results showed that: prostaglandin synthase inhibitor dexamethasone, ibuprofen and indomethacin, bradykinin receptor B2 antagonist HOE 140, platelet activating factor antagonist WEB2086, histamine H1 receptor antagonist diphenhydramine And histamine H2 receptor antagonist cimetidine, were significantly inhibited endotoxin-induced CGRP release, 5-HT receptor antagonist ICS205 930 but no significant effect. This suggests that endotoxin-induced release of CGRP is mediated through inflammatory mediators of prostaglandins, bradykinin, platelet activating factor and histamine, and that blocking or reducing the production of inflammatory mediators is expected to reduce the excessive release of CGRP during endotoxemia.