白细胞介素-2引起离体大鼠主动脉环舒张及其作用机制

Interleukin-2 induced endothelium-dependent relaxation of rat thoracic aorta

本文旨在研究白细胞介素 2 (interleukin 2 ,IL 2 )对离体大鼠胸主动脉环收缩张力的作用及其可能机制。采用累积加药法 ,检测IL 2对去氧肾上腺素 (PE)和KCl预收缩的胸主动脉环收缩张力的影响。结果表明 ,IL 2 (1、10、10 0、10 0 0U/ml)对PE (10 μmol/L)预收缩的内皮完整血管环产生浓度依赖性的舒张作用 ,而对KCl(12 0mmol/L)预收缩的血管无作用。去除内皮后 ,IL 2的舒张作用被取消。用一氧化氮合酶抑制剂L NAME (0 1mmol/L)和鸟苷酸环化酶抑制剂亚甲蓝 (10 μmol/L)预处理 ,均可阻断IL 2的舒张血管作用。用环氧合酶抑制剂吲哚美辛 (Indo,10 μmol/L)预处理可阻断IL 2的血管舒张作用。从上述观察结果推论 ,IL 2通过NO

Interleukin 2 ( IL 2 ) therapy often results in potentially life threatening side effects including hypotension. However, the mechanism has not been completely elucidated. In order to determine whether IL 2 modifies vascular tone, we investigated the effect of IL 2 on rat thoracic aorta rings and the underlying mechanisms. Effects of IL 2 on the contraction of high KCl and phenylephrine (PE) preconstricted rat thoracic aorta with or without endothelium were determined by organ bath technique. To explore the mechanism, nitric oxide synthase inhibitor L N ( G ) nitroarginine methyl ester ( L NAME), guanylyl cyclase inhibitor methylene blue, and cyclooxygenase inhibitor indomethacin were used. IL 2 (10～1000 U/ml) caused concentration dependent relaxation of aorta rings preconstricted with PE (10 μmol/L) in endothelium intact rings, but had no effect on KCl (120 mmol/L) preconstricted rings. Removal of the endothelium, or pretreatment with L NAME (0 1 mmol/L) or methylene blue (10 μmol/L) or indomethacin (10 μmol/L), inhibited the relaxation of IL 2 . The results indicate that the relaxation by IL 2 in rat aorta ring is endothelium dependent and is possibly mediated by the NO guanylyl cyclase pathway and cyclooxygenase dependent pathway.