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目的：观察降钙素基因相关肽（ＣＧＲＰ）在大鼠冷束缚应激过程中的动态改变及作用。方法：制作大鼠冷束缚应激动物模型，检测应激前及应激后２，４，６，８ｈ大鼠血浆ＣＧＲＰ含量；不同实验组大鼠，应激前用吲哚美辛（５ｍｇ／ｋｇ，皮下）、Ｌ－硝基－精氨酸甲酯（Ｌ－ＮＡＭＥ，５ｍｇ／ｋｇ，颈静脉注射）、生理盐水（５ｍｌ／ｋｇ，颈静脉注射）预处理，检测应激２ｈ大鼠血浆ＣＧＲＰ含量、胃粘膜血流量（ＧＭＢＦ）、胃液ｐＨ值及粘膜溃疡指数（ＵＩ）。结果：大鼠应激６ｈ血浆ＣＧＲＰ含量升高（Ｐ＜０．０５），８ｈ显著升高（Ｐ＜０．０１）。用吲哚美辛和Ｌ－ＮＡＭＥ预处理后均可降低ＧＭＢＦ、升高ＵＩ（Ｐ＜０．０５）、刺激血ＣＧＲＰ升高。结论：大鼠冷束缚应激可导致粘膜严重损伤，血浆ＣＧＲＰ含量升高；阻断一氧化氮合酶及环氧化酶均明显加重粘膜损伤，促进血浆内ＣＧＲＰ含量升高
Objective: To observe the dynamic changes and the role of calcitonin gene related peptide (CGRP) during cold restraint stress in rats. Methods: Cold stress rat model was established, and plasma CGRP levels were measured before and 2, 4, 6 and 8 h after stress. Rats in different experimental groups were treated with indomethacin (5 mg / kg, subcutaneously), L-nitro-arginine methyl ester (L-NAME, 5 mg / kg, jugular vein injection) and normal saline (5 ml / CGRP content, gastric mucosal blood flow (GMBF), gastric juice pH and mucosal ulcer index (UI). Results: After 6h of stress, the content of CGRP in rats increased (P <0.05) and increased significantly at 8h (P <0.01). Pretreatment with indomethacin and L-NAME decreased GMBF, increased UI (P <0.05), and stimulated the increase of blood CGRP. CONCLUSIONS: Cold restraint stress can cause severe mucosal injury and increase plasma CGRP levels. Blockade of nitric oxide synthase and cyclooxygenase both significantly aggravate mucosal injury and increase plasma CGRP levels