高碳酸抑制兔离体脑动脉缺氧性收缩

Carbon Dioxxide Inhidited the Hypoxic Vasoconstriction in Isolated Rabbit Basillar Arteries

在离体兔基底动脉观察了ＣＯ_２、ｐＨ值对血管缺氧反应的影响。在以５－羟包胺（１０^（－６）ｍｏｌ／Ｌ）预收缩后，缺氧使血管张力升高１１４．８７±４０．７５ｍｇ，Ｔ％为４８．６２±１２．１１（ｎ＝５１）。去内皮对缺氧性收缩无影响。随浴槽液中ＣＯ_２浓度增加，缺氧性收缩幅度减弱，在Ｐ_∞_２为８．００、９．３３、１０．６７ｋＰａ时，Ｔ％仅分别为３８．３０±５．３６％（ｎ＝１１）、３２．２５±７．７６％（ｎ＝１３）、２９．９０±９．２６％（ｎ＝１１），较对照值（Ｐ_∞_２＝５．３３ｋＰａ）均有显著差异（Ｐ＜０．０１）。ｐＨ７．３～７．７时血管缺氧反应无显著变化。一氧化氮合成酶抑制剂Ｌ—ＮＮＡ（１０~６）可抑制血管的缺氧收缩反应，也抑制了不同ＣＯ_２浓度对缺氧反应的影响，结果提示ＣＯ_２可能经促血管分泌ＮＯ的功能而抑制了缺氧性收缩。

The effects of carbon dioxide (CO2) and pH on hypoxic vasoconstriction (HVC) were studied in isolated rabbit Basillar arterial rings (BAR). BAR were suspended in Krebs-Hansleite solution for isometric recording. Hypoxia was induced by changing the bubbling gas mixture in the chamber from 95%O2-5% CO2 to 95%N2-5%CO2. Hypoxia caused contraction (tension increment: 114. 87±40. 75 mg, n＝51) in BAR precons-tricted with serotonin (10(-6)mol/L) and HVC remained unehange when the endothelium was removed from BAR. The increase of CO2 concentration in the chamber inhibited the HVC in BAR, But the change in pH had no significant influence on HCV. NG-Nitro-L-Arginine (L-NNA, 10(-6)mol/L), the inhibitor of Nitro Oxide (NO) synthase not only inhibited the HVC in BAR, but also inhibited the effects of high concentration of CO2 on HVC. The results showed that the high concentration of CO2 can induce the release of NO from BAR to inhibit the HVC.