束缚应激抑制大鼠血小板L-精氨酸转运

Restraint stress inhibits L-arginine transportation of platelets in rats

目的观察束缚应激7h对大鼠血小板L-精氨酸/一氧化氮(L-Arg/NO)通路的影响,并探讨其影响机制。方法制备大鼠束缚-浸水(waterimmersionrestraint,WIR)应激7h模型,采用Greiss法测定血小板孵育液中亚硝酸盐(NO2-)含量;同位素示踪法检测血小板一氧化氮合酶(NOS)活性及L-Arg转运。结果WIR应激组较对照组血小板NOS活性降低45%;L-Arg最大转运速率(Vmax)减少30%,Km增加38%(P<0.01),转运效率(Vmax/Km)减少50%(P<0.05);孵育液NO2-含量减少53%(P<0.01);胃溃疡出现。结论WIR应激损伤血小板L-Arg/NO通路,抑制血小板L-Arg转运和NOS活性,减少血小板NO生成。

[Objective] To investigate the mechanism of platelet function caused by water-irmnersion- restraint （WIR） stress in rats, by observing the change of the L-arginine/nitric oxide （L-Arg/NO） pathway of platelets. [Methods] Male Sprague-Dawley rats underwent water-irmnersion-restrain（WIR） stress for 7 h, detected the ulcer index（Ur） of stomach by Guth method; measured the nitrite production by Greiss assay; detected NOS activities and L-arginine transportation by isotope tracer method in each group. [Results] Compared with control rats, stressed rats showed decreased NOS activities by 45%; Vmax of L-arginine transportation was decreased by 30%, Km values was elevated by 38%（P 〈0.01, respectively）, transport efficiency （Vmax/Km） was reduced by 50%（P 〈0.05）; the nitrite production was also decreased by 53% （P 〈0.01）; gastric ulcers induced by WIR stress in rat stomach. [Conclusion] WIR stress, which had been damaged L-arginine/NO pathway of platelets, lowered L-arginine uptake, NOS activities and nitric oxide.