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作 者:洪志刚[1] 王迪浔[1] 刘声远[1] 张少华[1] 孙秉庸[2]
机构地区:[1]同济医科大学卫生部呼吸系疾病重点实验室病理生理室,武汉430030 [2]第三军医大学病理生理学教研室,重庆400038
出 处:《同济医科大学学报》2000年第2期93-96,共4页Acta Universitatis Medicinae Tongji
基 金:国家自然科学基金!重点资助项目 (No.39730 190 )
摘 要:探讨了慢性低压低氧对大鼠肺血管反应性的影响 ,以及前列腺素在其中的作用。结果表明 :1离体肺动脉在急性低氧时先收缩后舒张。大鼠经慢性低氧 15 d、 30 d后离体肺动脉对急性低氧所致收缩反应 (+Δ TIH)较各自对照组均明显降低 [(10 .11± 9.5 6 ) mg、 (14.5 7± 10 .0 2 ) m g Vs (2 7.15± 12 .0 9) mg、 (2 7.86± 13.0 7) mg,P<0 .0 1) ];舒张反应 (-Δ TIH)较各自对照组均明显增强 [(14.18± 5 .14) mg、 (2 6 .35± 11.74) m g Vs (9.39± 7.12 ) mg、 (8.99± 7.32 ) mg]。 2慢性低氧 15 d、 30 d后单位重量肺血管对高钾收缩反应 (ΔTK0 )为 [(10 5 .4± 32 .2 ) m g、 (113.9±2 8.3) m g],分别低于各自对照组 [(132 .7± 30 .3) m g、 (133.1± 34 .2 ) mg]。 3消炎痛可增强低氧性肺血管收缩反应 ,慢性低氧 30 d组增强百分比为 (148.87± 5 7.0 8) % ,明显高于其对照组 (5 9.0 2± 2 4.5 2 ) % ,P<0 .0 1。提示 :慢性低氧降低肺血管反应性可能是由于肺血管平滑肌的收缩性降低以及前列腺素对 HPV的调节作用增强所致。The effects of chronic hypobaric hypoxia on pulmonary vasoreactivity in rat and the role of prostaglandin were studied. The results showed: ① The response of intrapulmonary artery rings to acute hypoxia consisted of a transient contraction followed by a relaxation and a sustained contraction. The transient contraction reactivity was significantly attenuated and the relaxation reactivity significantly potentiated by exposure of the rats to chronic hypobaric hypoxia for 15 d (CH15 group) and for 30 d (CH30 group). The contractile responses to acute hypoxia (+ΔTIH) in the group CH15 and CH30 were significantly lower than those of respective control group [(10.11±9.56) mg, (14.57±10.02) mg Vs (27 15±12 09) mg, (27.86±13.07) mg, P <0.01];The following relaxative response (-ΔTIH) were significantly higher than those of respective control groups [(14.18±5.14) mg, (26.35±11.74) mg Vs (9.39±7.12) mg, (8.99±7.32) mg]. ② The contractile response of each unit weight of intrapulmonary artery rings to KCl in group CH15 and CH30 (ΔTK 0) was (105.4±32.2) mg and (113.9±28.3) mg respectively,significantly lower than that of respective control groups [(132.7±30.3) mg, (133 1±34.2) mg]. ③Indomethacin could enhance hypoxic pulmonary vasoconstriction and the enhancement in group CH30 was much higher than that of the control group [(148.87±57.08) % Vs (59.02±24.52) %, P <0.01]. These results suggest that the mechanism of chronic hypoxia attenuating hypoxic pulmonary vasoconstriction might be that pulmonary artery smooth muscle contractility was reduced and the regulatory effects on hypoxic pulmonary vasoconstriction inhanced by prostaglandin.
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