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作 者:宋为[1] 李世强[1] 蔡英年[1] 邓希贤[1] 梁兵[1] 齐保申[1] 龚伊红[1] 董继红[1]
机构地区:[1]中国医学科学院基础医学研究所生理学研究室,中国医学科学院基础医学研究所病理学研究室,西藏医学科学研究所
出 处:《中国应用生理学杂志》1994年第3期193-197,共5页Chinese Journal of Applied Physiology
摘 要:本实验对慢性减压缺氧(5000m)过程中肺动脉ACh内皮依赖性舒张反应作了动态观察,并结合分析了其与内皮超微结构和肺动脉压演变的关系。结果表明,缺氧3─21d,平均肺动脉压(mPAP)显著递增(P<0.05─0.001),而缺氧40d组基本与缺氧21d组持平,未再进一步升高。缺氧1d组,各ACh浓度(10-10、10-9、10-7、10-6、10-5mol/L)引起的内皮依赖性舒张反应明显受抑(P<0.05─0.001)。缺氧7d组,舒张反应的受抑程度与缺氧1d组基本相同;但ACh10-5mol/L引发的反应则较缺氧1d时更弱。缺氧21d和40d组,ACh10-6和10-5mol/L引起的舒张反应,尽管仍显著低于对照,但却基本上高于缺氧1d和7d组。其余各浓度ACh引发的反应则已趋于恢复至对照水平。电镜观察,缺氧1─14d肺动脉内皮呈逐渐加重的水肿变性;缺氧21─40d内皮水肿消失,代之出现渐趋活跃的内皮增生。结果提示,随缺氧时间延长,因内皮从损伤逐渐加重到出现代偿适应,可能存在相应的内皮舒张因子由释放减少到有所恢复的动态变化过程,并对整体肺动脉压有一定程度的影响。The pulmonay arterial endothelium-dependent relaxation evoked by ACh in the course of chronic hypobaric hypoxia (5000m) was observed and its relation with the changes of endothelial ultrastructure and pulmonary arterial pressure (PAP) was analysed. The results were as follows,Mean pulmonary arterial pressure (mPAP) continuously rose from 3 to ZI days of hypoxic exposure, but on the 4lst day, it was almost at the same level as that on the 21st day. On the first exposure day, the endothelium-dependent relaxation evoked by ACh was obviously depressed. On the 7th day, the relaxation remained almost at the same level as that on the first day. In the groups of ZI- and 40-day exposure, the relaxation tended to recover from depression. Ultrastructural examination revealed a gradually aggravating edema of the endothelium from 1 to 14 days of exposure, which disappeared with the occurrence of endothelial proliferation from 21st to 40th days.The results suggest that along with the prolongation of hypoxic exposure, the release of endothelium-derived relaxation factors (EDRFs) changes from reduction to increase with the adaptation of endothelium and such change may have certain effect on PAP. *Institute of Medical Sciences, Tibet, 850000
分 类 号:R331.37[医药卫生—人体生理学]
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