摘要
应用生物测定法观察黄嘌呤(X)-黄嘌呤氧化酶(XO)系统产生的氧自由基对正常、缺氧(5000m,10d)Wistar大鼠肺内动脉环张力的影响及内皮细胞在其中的作用。发现XO在一定浓度范围内产生的氧自由基可引起肺内动脉剂量依赖性收缩。正常鼠肺内动脉去内皮或加内皮舒张因子 (EDRF) 灭活剂后,此剂量依赖性收缩明显增强。慢性缺氧大鼠肺内动脉无论内皮完整与否,上述收缩反应均增强。提示缺氧使内皮细胞和(或)EDRF的功能受到损害。应用超氧化物歧化酶(铜锌SOD),在正常或缺氧鼠肺内动脉上可分别加强或恢复内皮细胞抑制氧自由基的缩血管作用。提示慢性缺氧时,内皮细胞和(或)EDRF受到超氧阴离子的严重破坏,这一机制可能在缺氧性肺动脉高压的形成中起重要作用。
The system of xanthine (X, 10-4mol/L) plus xanthine oxidase (XO, 0.001, 0.002, 0.003, 0.01, 0.03U / ml) was used to study the effect of oxygen-derived free radicals on tension of intrapulmonary artery and the role of endothelial cells in this response. Male Wistar rats were divided into chronic hypoxic group (H) placed in a hypobaric chamber (5 000m, 10, n = 7) and air-breathing control group (C, n= 10). Rings (3-4mm in length) of left intrapulmonary artery (A 1) with (+endo, A rings) and without (-endo, B rings) endothelium from H and C groups were suspended in Krebs solution (pH = 7.40) gased with air+5% CO2 (37℃). Contraction of the rings induced by oxygen-derived free radicals was expressed as percent of the response to 60mmol / L KC1.The results showed that oxygen-derived free radicals caused concentration-dependent contraction of intrapulmonary artery rings in both groups. In C group, the contraction was augmented more significantly in B rings than in A rings, suggesting that endothelial cells inhibited contraction induced by oxygen-derived free radicals. Reduced hemoglobin (1.667×10-6mol/ L) abolished the inhibitory action of endothelium, while superoxide dismutase (SOD, 150 U/ml) enhanced it significantly in A rings. In contrast, reduced hemoglobin and SOD did not affect obviously the contraction of B rings. These data suggested that endothelium could inhibit contraction of vascular smooth muscle by releasing endothelium-derived relaxing factor (EDRF) and there might be close relationship between EDRF and superoxide anion. In H group, contraction to oxygen-derived free radicals showed no significant difference between A and B rings. Addition of SOD (150U/ml) reduced obviously contraction in A rings, but not in B rings. It shows that chronic hypoxia may abolish the inhibitory effect of endothelium and superoxide anion may be involved in this mechanism. In conclusion, it is suggested that the relationship between EDRF and superoxide anion should be emphasized in studying the development of chronic hypoxic pulmonary hypertension.
出处
《中国应用生理学杂志》
CAS
CSCD
1992年第2期106-110,共5页
Chinese Journal of Applied Physiology
基金
国家自然科学基金
关键词
氧自由基
肺内动脉
内皮细胞
缺氧
endothelium-derived relaxing factor
chronic hypoxia
intrapulmonary artery
oxygen-de-rived free radicals
