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作 者:牟信兵[1] 李素芝[1] 高钰琪[2] 刘福玉[2] 叶刚林[1] 汤红亚[1] 朱旦[3] 周小波[1] 陈光林[1]
机构地区:[1]西藏军区总医院全军高山病防治研究中心,西藏拉萨850003 [2]第三军医大学高原医学系,重庆400038 [3]重庆医科大学检验系,重庆400000
出 处:《中国病理生理杂志》2003年第8期1106-1108,共3页Chinese Journal of Pathophysiology
基 金:全军"十五"指令性课题 (0 1L0 6 2 )
摘 要:目的 :探讨高原肺水肿的发病机理。方法 :采用右心漂浮导管检测法 ,对 9例高原肺水肿患者及 9例同海拔高原健康人的血流动力学指标进行了检测 ,同时也观察了吸入纯氧对高原肺水肿患者血流动力学的影响。结果 :高原肺水肿患者发病时 ,肺动脉平均压、肺血管阻力、心脏指数均明显高于同海拔高度健康人 ,而患者肺动脉楔压 ,右心房压力同对照组相比 ,未见显著差异 ;吸氧后 ,高原肺水肿患者心率、肺动脉平均压力 ,肺血管阻力及心脏指数均较吸氧前明显下降 ,特别是肺动脉平均压及肺血管阻力下降尤为明显 ,肺动脉平均压力在吸氧 1min后即明显下降 ,吸氧 5min后 ,下降至最低值 ,但吸氧 2 0min后仍未达对照组水平。结论 :高原肺水肿是非心源性肺水肿 ,肺动脉高压在其发病中起重要作用。AIM: To explore the pathogenic mechanism of high altitude pulmonary edema(HAPE). METHODS: Haemodynamic changes and effects of 100 percent oxygen breathing were measured by Swan-Ganz thermistor catheters, high altitude healthy volunteers were served as controls. RESULTS: The important features of haemodynamic changes in HAPE: (1)Pulmonary arterial pressure was raised; (2)Pulmonary arterial resistance and cardiac output were raised; (3)Pulmonary artery wedge pressures and right atrial pressure were normal; (4)Pulmonary arterial pressure and resistance were induced by oxygen breathing. CONCLUSIONS: The normal pulmonary artery wedge pressures with a high cardiac output indicated that HAPE was recognized as a form of noncardiogenic pulmonary edema. The pulmonary hypertension may play an important role in the development of HAPE.
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