Berkenkopf J W, Weichman B M
Department of Pharmacology, Ayerst Laboratories Research, Princeton, N.J.
Pharmacology. 1987;34(6):309-25. doi: 10.1159/000138285.
At 4 h following induction of pleural inflammation in rats using either an immune stimulus (reverse passive Arthus reaction, RPAR) or a chemical stimulus (carrageenan), the cellular infiltration and fluid accumulation responses were quantitated. The bell-shaped antigen (BSA) dose-response curve describing the fluid response was increased upward as the anti-BSA dose was increased from 0.25 to 1 mg, whereas the dose-response curve for cellular infiltration was both shifted upward and to the right. Both nonsteroidal anti-inflammatory drugs and a mixed lipoxygenase-cyclooxygenase inhibitor (BW 755C) preferentially inhibited fluid accumulation in RPAR pleurisy elicited with 5 mg BSA and 1 mg anti-BSA and in carrageenan pleurisy. In contrast, these drugs inhibited cellular infiltration preferentially in RPAR pleurisy elicited with 1 mg BSA and 1 mg anti-BSA. These results demonstrate that the fluid and cellular responses in rat pleural inflammation can be differentially regulated by anti-inflammatory drugs depending upon the doses of antigen and antibody employed in RPAR pleurisy and the identity of the inflammatory stimulus.
在使用免疫刺激(反向被动阿瑟斯反应,RPAR)或化学刺激(角叉菜胶)诱导大鼠胸膜炎症4小时后,对细胞浸润和液体蓄积反应进行定量分析。描述液体反应的钟形抗原(牛血清白蛋白,BSA)剂量反应曲线随着抗BSA剂量从0.25毫克增加到1毫克而向上移动,而细胞浸润的剂量反应曲线则向上和向右移动。非甾体抗炎药和一种混合的脂氧合酶 - 环氧化酶抑制剂(BW 755C)优先抑制用5毫克BSA和1毫克抗BSA引发的RPAR胸膜炎以及角叉菜胶胸膜炎中的液体蓄积。相比之下,这些药物在使用1毫克BSA和1毫克抗BSA引发的RPAR胸膜炎中优先抑制细胞浸润。这些结果表明,大鼠胸膜炎症中的液体和细胞反应可由抗炎药物根据RPAR胸膜炎中使用的抗原和抗体剂量以及炎症刺激的类型进行差异调节。