论文部分内容阅读
我们以前的工作表明，动物内毒素血症和失血性休克以及人的败血症时血浆ＣＧＲＰ含量明显增多，它的主要来源之一是血管。本实验的目的是探讨是否内毒素可直接使离体大鼠肠系膜动脉床含ＣＧＲＰ的外周神经释放ＣＧＲＰ增加。结果显示内毒素（１０－１００μｐ／ｍｌ）灌流引起ＣＧＲＰ时间和剂量依赖性的释放，内毒素（５０μｐ／ｍｌ）灌注后１０－１５ｍｉｎ时，ＣＧＲＰ释放达高峰，该时释放量为基础状态时的２０倍。经反相高压液相分析证明，ＣＧＲＰ免疫活性的峰位与人工合成大鼠ＣＧＲＰ标准品的峰位吻合。以辣椒素（感觉神经选择性毒剂）预灌流或钌红（钙致细胞内钙池释放阻断剂）均可使上述内毒素引起的ＣＧＲＰ释放分别抑制９０％和６５％。在灌流液无钙时内毒素致ＣＧＲＰ释放的作用被抑制８０％。以上结果提示：内毒素可直接引起ＣＧＲＰ从大鼠肠系膜动脉床释放，来源主要为辣椒素敏感的感觉神经。释放依赖于细胞外钙离子的存在以及Ｃａ~（２＋）进入神经细胞后引起的对钌红敏感的细胞内钙池Ｃａ~（２＋）动员。
Our previous work showed that plasma CGRP levels were significantly increased in animal endotoxemia and hemorrhagic shock as well as in human sepsis, one of the major sources of which is blood vessels. The purpose of this experiment is to investigate whether endotoxin directly increases CGRP released from CGRP-releasing peripheral nerves in isolated rat mesenteric arterial beds. The results showed that the perfusion of endotoxin (10-100μ p / ml) caused a time-and dose-dependent release of CGRP. The release of CGRP peaked at 10-15min after endotoxin (50μβ / 20 times. The reversed-phase high-pressure liquid phase analysis showed that the peak position of CGRP immunocompetence was consistent with the peak position of synthetic CGRP standard. Pretreatment with capsaicin (sensory nerve-selective agent) or ruthenium red (calcium-induced intracellular calcium channel blocker) inhibited the endotoxin-induced CGRP release by 90% and 65%, respectively. The effect of endotoxin-induced CGRP release was inhibited by 80% in the presence of calcium-free perfusate. The above results suggest that endotoxin can directly release CGRP from rat mesenteric artery bed and the main source is capsaicin-sensitive sensory nerve. The release depends on the presence of extracellular calcium ions and Ca2 + mobilization of intracellular calcium cells which is sensitive to ruthenium red after Ca2 + entry into nerve cells.