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目的:研究缺氧引起的血管收缩是否与血管内皮细胞释放内皮素(ET)有关.方法:95%O2+5%CO2混合气体换成95%N2+5%CO2引起急性缺氧,描记猪基底动脉环的张力变化.结果:在基础张力条件下和由ET3nmol·L-1引起收缩时,缺氧分别使基底动脉张力增加021g±008g和024g±009g.当ET浓度从100nmol·L-1增加到300nmol·L-1时,动脉的张力不进一步增加,此时急性缺氧仍使张力进一步增加016g±010g.过氧化氢酶800,2400kU·L-1明显降低缺氧引起的收缩,抑制率分别为33%±7%和47%±9%.结论:缺氧引起的血管收缩与内皮细胞释放过氧化氢有关
Objective: To investigate whether hypoxia-induced vasoconstriction is associated with the release of endothelin (ET) from vascular endothelial cells. Methods: Acute hypoxia was induced by changing 95% O2 + 5% CO2 mixed gas into 95% N2 + 5% CO2, and the changes of the tension of pig basilar artery rings were described. RESULTS: Hypoxia increased basilar artery tension by 021g ± 008g and 024g ± 009g, respectively, under basic tension and induced by ET3nmol·L-1. When the concentration of ET increased from 100nmol·L-1 to 300nmol·L-1, the tension of the artery did not increase further. At this time, the acute hypoxia increased the tension further by 0.16 ± 0.10g. Catalase 800,2400 kU · L-1 significantly reduced hypoxia induced contraction, the inhibition rates were 33% ± 7% and 47% ± 9%. Conclusion: Hypoxia-induced vasoconstriction is associated with the release of hydrogen peroxide from endothelial cells