【摘要】 研究消炎痛及乙胺嗪对家兔肺、脑血管和大鼠脑微动脉缺氧反应的影响。发现吸入10％氧使家兔肺血管阻力(PVR)增加,脑血管阻力(CVR)降低,大鼠脑微动脉扩张。用消炎痛明显增强家兔缺氧性肺、脑血管反应。△PVR％由用药前26.6±16.7％增至44.2±7.7％;△CVR％则由一12.9±4.5％减至-30.7±4.7％;大鼠微动脉直径增大率(△D％)由用药前28.2±2.0％增至41.3±5.8％;用乙胺嗪则使缺氧时△PVR％由 84.6±18.1％降至 23.8±8.5％;△CVR％由-16.7±4.5％变为 6.9±2.8％;△D％由 29.7±5.8％减至 25.6±5.0％。结果表明前列腺素在缺氧性肺血管收缩反应及脑血管扩张反应中起调节作用,而白三烯则在缺氧性肺血管收缩反应中起介导作用。更多还原

【Abstract】 The effects of diethylcarbamazine (DEC) and indomethacin (IND) on acute hypoxic pulmonary vasoconstriction (HPV) and hypoxic cerebral vasodilation (HCVD) were studied in rabbits and rats. It was found that the alveolar hypoxia led to an increase in pulmonary resistance (CVR) in rabbits and caused cerebral arteriolar dilation in rats. HPV and HCVD of rabbits were potentiated after the administration of IND, the percentage increment in PVR (△PVR%) induced by hypoxia increased significantly from 26. 6 ± 6. 7% to 44. 2 ±7. 7%; and the percentage increment decreased in CVR (CVR%) from - 12. 9 ± 4. 5% to - 30. 7 ±4. 7% ; and the percentage increment in the diameter of rat cerebral arteriole (D%) increased from 28. 2±2. 0% to 41. 3±5. 8%. On the contrary, DEC decreased the hypoxia-induced PVR% from 84. 6±18. 1% to 23.8 ± 8. 5%, △CVR% from -16.7 ± 4-5% to 6.9 ±2.8%, and △D% from 29.7± 5.8% to 25.6 ±5.0%. These results showed that prostaglandins might play a role of modulator in HPV and HCVD; while leukotriene act as a mediator in HPV. The probable michanism of the reduction in HCVD and DEC is discussed.更多还原