缝隙连接阻断剂1-庚醇对血红蛋白诱导兔离体基底动脉环痉挛的抑制作用

Inhibitive effect of gap junctional blocker 1-heptanol on oxyhemoglobin-induced contraction in isolated rabbit basilar arteries

目的 探讨缝隙连接在脑血管痉挛中可能发挥的作用。方法 通过兔离体基底动脉环试验,观察缝隙连接阻断剂1-庚醇(heptanol)对氧合血红蛋白(OxyHb)和高K+引起血管收缩的影响。结果10^(-4)mol/L OxyHb和60 mmol/L K+引起动脉环收缩后,累积加入10^(-4)-10^(-2)mol/Lheptanol可以显著降低其收缩程度,并呈浓度依赖关系。当浓度为500μmol/L时,OxyHb引起的血管收缩幅度下降60%,1 mmol/L时几乎完全抑制OxyHb引起的持续收缩。同浓度的heptanol对OxyHb致痉的抑制作用比对K+致痉的抑制作用强。heptanol(≥3×10^(-4)moL/L)预处理动脉环后,能有效抑制OxyHb引起的血管收缩(P<0.01)。结论 缝隙连接阻断剂heptanol能显著抑制OxyHb对脑血管的致痉作用,缝隙连接在脑血管痉挛中可能发挥重要作用。

Objective To investigate the role of gap junctions in cerebral vasospasm. Methods The effect of heptanol, a blocker of gap junctions, on the OxyHb-induced or K+ -induced contraction of isolated rabbit basilar arteries were observed by an isometric tension-record method. Results 10^(-4)- 10^(-2) mol/L heptanol significantly inhibited the contraction of basilar arterial rings induced both by 10^(-4) mol/L OxyHb and 60 mmol/L K + . The magnitude of the heptanol-induced relaxation was dose-dependent. In 500 μmol/L heptanol, the magnitude of the OxyHb-induced vasocontraction was reduced to 60% , while in 1 mmol/L heptanol, it was almost completely inhibited. The inhibitory effect of heptanol on the K + -induced vasocontraction was also observed but it was not so strong as that on the OxyHb-induced. After pretreated arterial rings for ten minutes, heptanol (≥3×10^(-4) mol/L ) was significantly decreased in their responses to the OxyHb-induced contraction (P < 0. 01 ) . Conclusion Heptanol might significantly inhibite the OxyHb-induced contraction of rabbit basilar arteries in vitro. The gap junctions might play a pathophysiological role in the cerebral vasospasm.