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我们以前的工作表明在内毒素和失血性休克时ＣＧＲＰ释放入血循环。本实验在离体大鼠肠系膜动脉床灌流的模型上，发现低ＰＨ、高乳酸、高氯化钠和高蔗糖溶液均能直接引起ＣＧＲＰ释放增加，进一步应用辣椒素预灌流，ＣＧＲＰ释放的作用被抑制，同时ＣＧＲＰ释放可以被一种钙引起的细胞内钙池释放阻断剂钉红所抑制，而且应用无钙的低ＰＨ，高乳酸及高渗液就不能引起ＣＧＲＰ释放增多，实验结果提示：上述理化因子导致ＣＧＲＰ从大鼠肠系膜动脉床的释放主要是通过刺激对辣椒素敏感的感觉神经，这一释放依赖于细胞外钙离子的存在以及Ｃａ２＋进入细胞引起的对钉红敏感的细胞内钙池Ｃａ２＋释放。
Our previous work showed that CGRP is released into the bloodstream during endotoxin and hemorrhagic shock. In this study, we isolated rat mesenteric artery bed perfusion model and found that low PH, high lactate, high sodium chloride and high sucrose solution can cause a direct increase in CGRP release, further application of capsaicin preperfusion, the role of CGRP release Inhibition, and CGRP release can be inhibited by a calcium-induced intracellular calcium release blocker nails red, and calcium-free low PH, high lactate and hypertonic solution can not cause increased CGRP release, the experimental results suggest that: The above physicochemical factors lead to the release of CGRP from the rat mesenteric artery bed by stimulating the capsaicin-sensitive sensory nerves. This release is dependent on the presence of extracellular calcium ions and Ca2 + entry into the cell-induced nail-red sensitive intracellular calcium Pool Ca2 + release.