白细胞介素-2引起离体大鼠主动脉环舒张及其作用机制

本文旨在研究白细胞介素－2（interleukin-2,IL-2）以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、100、1000U／ml）对PE（10μmol/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 (120mmol/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（10μmol/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,10μmol/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－鸟苷酸环化酶和环氧合酶途径产生内皮依赖的血管舒张作用。

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

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 micromol/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 micromol/L) or indomethacin (10 micromol/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.