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引起的通透性增加。研究发现，内毒素可引起大鼠对Des-Arg9-Bradykinin的降压和收缩反应。从拮抗剂和蛋白质合成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，内毒素处理大鼠巨噬细胞也可诱导环氧合酶-2的表达。采用大鼠腹腔或胸膜腔内注射内毒素的方法建立炎症模型。

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.