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增加的过程。结果发现，在预先用内毒素处理的大鼠中，对des-Arg 9-缓激肽诱导了膨胀和收缩反应。从蛋白质合成的拮抗剂和抑制剂的实验结果可以得出结论，这两种反应都是通过新诱导的B1受体介导的。此外，环氧合酶-2也诱导大鼠巨噬细胞与内毒素处理。腹腔内或胸腔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.