The development of inflammatory models with endotoxin and its evaluation

结果表明，缓激肽可能参与了大鼠皮内注射内毒素后通透性的增加。我们发现，先前给内毒素治疗的大鼠对去- arg9 -缓激肽有降压和收缩反应。从蛋白合成拮抗剂和抑制剂的实验结果来看，这两种反应都是通过新诱导的B1受体介导的。此外，内毒素处理大鼠巨噬细胞也能诱导环氧合酶-2。并通过腹腔或胸膜内注射内毒素建立大鼠炎症模型。

It was shown that bradykinin might involve in the permeability increase with intradermally injected endotoxin in rats. It was found that the hypotensive and contractile responses to des-Arg9-bradykinin were induced in rats previously treated with endotoxin. From the experimental results with antagonists and inhibitors of protein synthesis, it could be concluded that both responses mediated via newly induced B1 receptors. Furthermore, cyclooxygenase-2 was also induced by treatment of rat macrophages with endotoxin. And the inflammatory models was established by the intraperitoneal or intrapleural injection of endotoxin into rats.