18-β甘草次酸抑制KCl对大鼠脑中动脉的收缩作用

Inhibited Effect of 18β-Glycyrrhetintic Acid on Vasoconstriction of KCl in Middle Cerebral Artery of Rat

为讨论缝隙连接阻断剂18β—GA在脑血管收缩反应中的可能作用。采用压力肌动图技术，在急性分离的Wistar大鼠的大脑中动脉（直径〈300μm），观察18β—GA干预前后不同浓度的收缩剂KCl对血管直径的影响。结果显示，KCl可以浓度依赖性的引起脑中动脉收缩，且30～80mmol／L引起的收缩与血管静息状态下的直径相比具有统计学差异（P〈0．05，n=7）。18βGA也可浓度依赖性的引起脑中动脉收缩，且10～100〉mol／L引起的收缩与未加药前相比具有统计学差异（P％0．05，n=8）。预灌流18β—GA（100／amol／L）后，50～80mmol／L KCl引起血管收缩幅度减小，拟合曲线下移，且差异具有统计学意义（P〈0．05，n=7）。由此可知：18B—GA可抑制KCl对脑血管的收缩作用，提示细胞问缝隙连接参与脑血管收缩活动。

Objective：To investigate the role of gap iunction in the middle cerebral artery vasoconstriction. Methods：Using the pressure myograph system to observe the changes of the diameter in acute separated middle cerebral artery（MCA, 〈300 microns） of Wistar rat after and before adding 18βGA（gap junction blockers）intervention in different concentrations of KCl. Results：KCl induced the MCA contraction in a concentration-dependent manner, and compared with the resting state, the MCA contraction induced by KCl（from 30 to 80 mmol/L）has significant difference（P〈0.05,n= 7）. 18βGA induced the MCA con- traction in a concentration-dependent manner,the MCA contraction induced by 18βGA（from 10 to 100 /xmol/L）has significant difference（P〈0.05 ,n= 8）. After pretreated by 1813GA（100 μmol/L）, the contraction amplitudes of MCA was obviously sup- pressed by KCl （50-80 mmol/L）, and the curve shift down, and this has significant difference（P〈0.05, n = 7）. Conclusion= 1813GA might significantly inhibit the contraction of MCA induced by KCl in Wistar rat,and intercellular gap junction communi cation participated in the activities of cerebrovascular contraction.