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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 CO_2 and pH on the vascular hypoxia were observed in isolated rabbit basilar artery. After precontracted with 5-hydroxybutylamine (10 -6 mol / L), hypoxia increased blood vessel tension by 114.87 ± 40.75 mg and T% by 48.62 ± 12.11 (n = 51). Endothelium has no effect on hypoxic contractions. With the increase of CO 2 concentration in the bath, the amplitude of hypoxia contractions was weakened, while the% T was only 38.30 ± 5.36% (n = 11) when P_∞_2 was 8.00, 9.33 and 10.67 kPa, respectively ), 32.25 ± 7.76% (n = 13) and 29.90 ± 9.26% (n = 11), respectively, which were significantly different from the control value (P_∞_2 = 5.33 kPa) .01). There was no significant change of hypoxia response at pH7.3 ~ 7.7. L-NNA (10-6), a nitric oxide synthase inhibitor, can inhibit the hypoxia-contractile response of blood vessels and also inhibit the effects of different CO 2 concentrations on hypoxia. The results suggest that CO 2 may be inhibited by the function of NO secretion by blood vessels Hypoxic contraction.