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本实验在离体灌流大鼠肠系膜动脉床研究内毒素引起降钙素基因相关肽（ＣＧＲＰ）释放的机制。内毒素（５０μｇ／ｍｌ）使ＣＧＲＰ释放增加１６倍，一氧化氮合成酶（ＮＯＳ）底物Ｌ－精氨酸（Ｌ－Ａｒｇ）能促进内毒素引起的ＣＧＲＰ释放（４１％）。ＮＯＳ抑制剂Ｎ￣Ｇ－硝基－Ｌ－精氨酸（Ｌ－ＮＮＡ）及鸟苷酸环化酶抑制剂甲基蓝（ＭＢ）能使内毒素的上述作用分别降低３５％与３６％，Ｌ－精氨酸（ｔ－Ａｒｇ）能逆转Ｌ－ＮＮＡ的作用。提示内毒素的作用机制中部分是通过一氧化氮引起细胞内ｃＧＭＰ升高而介导的。用化学方法破坏血管内皮细胞，Ｌ－ＮＮＡ与Ｌ－Ａｒｇ的上述作用依然存在。提示内毒素主要是激活血管周围感觉神经末梢的神经源ＮＯＳ，而非内皮源ＮＯＳ。环氧化酶抑制剂消炎痛（Ｉｎｄｏ）与布洛芬（Ｉｂｕ）也能使内毒素引起ＣＧＲＰ释放的作用分别降低３４％与３９％，但与Ｌ－ＮＮＡ的作用不能迭加。提示内毒素可能通过激活神经源ＮＯＳ进而引起环氧化酶活化而起作用。
In this study, the mechanism of endotoxin-induced release of calcitonin gene-related peptide (CGRP) was investigated in isolated rat mesenteric arterial bed. Endotoxin (50 μg / ml) increased CGRP release by a factor of 16 and L-arginine (L-Arg), a nitric oxide synthase (NOS) substrate, promoted endotoxin-induced CGRP release (41%). NOS inhibitors N-G-nitro-L-arginine (L-NNA) and guanylate cyclase inhibitor methyl blue (MB) reduced endotoxin effects by 35% and 36%, respectively, L-arginine (t-Arg) reverses the effect of L-NNA. It is suggested that the mechanism of action of endotoxin is partly mediated by the increase of intracellular cGMP caused by nitric oxide. Chemical damage to vascular endothelial cells, L-NNA and L-Arg the above effects still exist. It is suggested that endotoxin mainly activates NOS, a neurogenic nerve endothelium, but not endothelium-derived NOS. The effects of cyclooxygenase inhibitors indo and ibu also decreased endotoxin-induced release of CGRP by 34% and 39%, respectively, but the effect with L-NNA was not additive. This suggests that endotoxin may play a role in activating cyclooxygenase by activating neuronal NOS.