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目的:探讨链尿佐菌素(STZ)诱导的早期糖尿病C57BL(?)6J小鼠胸主动脉内皮依赖性舒张增强机制。方法:采用放免法测定糖尿病(DM)和对照(Control)组小鼠血清中前列环素(PGI_2)代谢物6-酮-前列环素F_((?)a)(6-keto-PGF_(1a))的含量,同时比较各组小鼠离体胸主动脉环对血管收缩剂、舒张剂的张力变化以及苯肾上腺素(PE)诱导的离体胸主动脉节律活动对各种阴断剂的反应性变化。结果:DM组小鼠血清6-ketoPGF_(1a)的含量较Control组显著增强[(1.8±1.0)μg/1.vs(0.5±0.3)μg/L,P<0.01];PE能够诱导DM和Control组小鼠离体胸主动脉环的节律活动,而且DM组的胸主动脉环节律活动振幅显著增大[(4.9±1.7)％vs(12±5)％,P<0.01]。DM组胸主动脉环对收缩剂PE和KCl 60 mmol/L的反应性比Control组显著增强;对内皮依赖性舒张剂乙酰胆碱(ACh)的反应也比Control组显著增强[(56±10)(?)vs(81±8)％,P<0.01].一氯化氮合酶抑制剂(L-NAME)和鸟苷酸环化酶抑制剂(LY-83583)分别能完全阴断Control组的PE诱导的节律活动和ACh的舒张效应,而在DM组只能部分阻断。L-NAME和吲哚美辛联用可以显著减小节律活动振幅和ACh的舒张效应(P<0.01)。钙激活型钾通道阻断剂(TEA)可以阻断内皮依赖性舒张因子(EDHF)的效应,它与L-NAME联用可以完全阻断节律活动?
AIM: To investigate the mechanism of endothelium-dependent relaxation of thoracic aorta induced by streptozotocin (STZ) in early-stage diabetic C57BL (?) 6J mice. Methods: The levels of 6-keto-prostacyclin F_ (?) A (6-keto-PGF_ (1a)), a metabolite of PGI_2 in serum of diabetic mice and control mice )). Meanwhile, the changes of vasoconstrictor and diastolic agents in isolated thoracic aorta rings of mice were compared, and the effects of phenylephrine (PE) -induced thoracic aortic rhythmicity on the activity of various ablative agents Reactivity changes. Results: The level of 6-ketoPGF_ (1a) in DM group was significantly higher than that in Control group [(1.8 ± 1.0) μg / L vs (0.5 ± 0.3) μg / L, P <0.01] Control group, the amplitude of rhythmic activity of thoracic aortic ring increased significantly in DM group [(4.9 ± 1.7)% vs (12 ± 5)%, P <0.01]. The reactivity of thoracic aortic rings to 60 mmol / L of PE and KCl in DM group was significantly higher than that of Control group, and the response to endothelium-dependent relaxation agent ACh was significantly higher than that of Control group [(56 ± 10) ( (81 ± 8)%, P <0.01]. L-NAME and guanylate cyclase inhibitor (LY-83583) PE-induced rhythmic activity and diastolic effects of ACh, while only partially blocked in the DM group. L-NAME combined with indomethacin significantly reduced the amplitude of rhythm activity and the diastolic effect of ACh (P <0.01). Calcium-activated potassium channel blocker (TEA) can block the effect of endothelium-dependent relaxation factor (EDHF), which in combination with L-NAME can completely block the rhythmic activity?