缝隙连接在肺动脉收缩中的作用

目的探讨缝隙连接在肺动脉收缩中可能发挥的作用。方法通过兔离体肺动脉环实验，观察缝隙连接阻断剂1-庚醇（Heptano1）对肾上腺素（Adr）和高K^＋起血管收缩的影响。结果1／μmol／L Adr引起的动脉环收缩后，加入0．1～5mmol／L Heptanol可以阻断肺动脉环收缩，舒张强度呈浓度依赖性；对K^＋引起的收缩Heptanol没有明显的舒张作用。Heptaol预处理动脉环也同样可以有效抑制Adr引起的血管收缩。结论缝隙连接阻断剂Heptanol能显著抑制Adr引起肺动脉血管环的收缩作用，这种舒张作用具有剂量依赖性、可逆性。但是对K^＋收缩没有明显的舒张作用。缝隙连接参与了肾上腺素收缩肺动脉血管环的作用。

The Role of Gap Junction in Pulmonary Vasoconstiction

Objective To investigate the role of gap junction in pulmonary vasoconstriction. Methods The effect of Heptanol, a blocker of gap junction, on the adnephrin-induced or K^＋ -induced contraction of isolated rabbit pulmonary arterial rings were observed by an isometric tension-record. Results 0.1-5 mmol/L Heptanol significantly inhibited the contraction of pulmonary arterial rings induced by 1 μmol/L adnephrin. The magnitude of the Heptanol-induced relaxation was does-dependent. After pretreated pulmonary arterial rings, Heptanol diminished the maximal amplitude of adnephrin-induced contraction. In contrast, there is no detectable effect on the magnitude of K^＋ -induced contractile responses. Conclusion Heptanol might significantly inhibite the adnephrin, but not K^＋ , induced contraction of rabbit pulmonary artery in vitro. The gap juncion might play an important role in pulmonary vasoconstriction.