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Endothelium-Independent Vasorelaxant Effect of Lidocaine in Rat Aortic Rings

机译:利多卡因对大鼠主动脉环的内皮依赖性血管舒张作用

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In the present study, lidocaine relaxed, in a concentration-dependent manner, the contractions induced by either phenylephrine or a high concentration of KCl (60 mM) in endothelium-intact rat aortic rings. Mechanical removal of endothelium did not significantly modify lidocaine-induced vasorelaxation. In endothelium-denuded aortic rings depolarized by 60 mM KCl, lidocaine inhibited Ca2+-induced contraction. Lidocaine also reduced the transient contraction elicited by phenylephrine in Ca2+-free medium. Pretreatment of endothelium-denuded aorta nonspecific K+with tetraethylammonium, a channel blocker, had no effect on the relaxant effect of lidocaine. These results indicate that lidocaine induces an endothelium-independent relaxation in rat aortic rings. The main mechanisms may include suppression in Ca2+through the voltage-sensitive Ca2+influx intracellular Ca2+channels and inhibition of release in the vascular smooth muscle cells.
机译:在本研究中,利多卡因以浓度依赖的方式舒张了由苯肾上腺素或高浓度的KCl(60 mM)诱导的在内皮完整的大鼠主动脉环中引起的收缩。机械去除内皮并没有明显改变利多卡因诱导的血管舒张。在被60 mM KCl去极化的内皮剥脱的主动脉环中,利多卡因抑制Ca 2 + 诱导的收缩。利多卡因还减少了去氧肾上腺素在不含Ca 2 + 的培养基中引起的瞬时收缩。用通道阻滞剂四乙铵预处理内皮剥脱的主动脉非特异性K + 对利多卡因的松弛作用没有影响。这些结果表明利多卡因在大鼠主动脉环中诱导内皮依赖性的松弛。其主要机制可能包括通过电压敏感的Ca 2 + 流入细胞内Ca 2 + 通道来抑制Ca 2 + 和抑制其释放。血管平滑肌细胞。

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