急性高原肺水肿心肌损伤机制的研究

目的探讨急性高原肺水肿（HAPE）患者发病初期的心肌细胞损害、细胞舒缩功能损害以及心电损害，同时测定急性缺氧期患者血管活性因子水平的变化，从血管舒缩因子失衡角度探讨HAPE的发病机制，为临床治疗和发病机制研究提供依据。方法分别采集急性高原肺水肿患者、高原健康、平原健康人3组人群样本血浆，分为HAPE组（n=21）、高原健康对照组（n=15），平原健康对照组（n=13），分别测定3组样本血浆促红细胞生成素（EPO）、血浆肌钙蛋白（cTNI）、氨基末端脑钠肽原（Nt-pro-BNP）水平，并将3组进行比较。结果HAPE组的EPO、VEGF为皮素ET-1高于平原对照组，差异有统计学意义（P〈0．05），而HAPE组与高原对照组间无统计学差异；HAPE组和平原、高原对照组血浆NO水平无统计学显著性差异。结论血管收缩物质增加，舒张物质减少以及由此导致的两种物质比例失衡，可能是HAPE发病的主要原因，不是某种收缩物质的增加或者舒张物质的减少作用的结果，HAPE存在心肌细胞损害和心功能受损。

THE PATHOGENIC STUDY ONMYOCARDIUMINJURY DUETO ACUTE HIGH ALTITUDE PULMONARY EDEMA

Objective To investigate the myocardial cell damage, systolic - diastofic and electrocardial function impairement on patients with acute high altitude pulmonary edema（HAPE） at primary level. And to investigate the pathogenic mechanisms of HAPE by study vasoacfive factors. Methods Blood samples werecollected from HAPE patients and healthy subjects from plateau and plain, and were grouped by their origin as HAPE group（n = 21 ）, plateau control（ n = 15 ）and plain control fn = 13 ）. The plasma level of EPO, cTNI and NT - pro - BNP were meas- ured and compared. Results The EPO, VEGF＆ETI in HAPE patients＇ plasma weresignificantly higher than pain control group （ P 〈 0. 05 ）. And no difference were found between the three groups in the levels of NO. Conclusion The mightbe structural, functional and cardio - electrical damage in myocardial cell in patients with HAPE, the methods including correcting hypoxia,improving cell metabolism condition and decnease load of heart could bring clinically beneficianl effects. And the increased levels of vasoconstrictors,decreased level of vasodialatition and the imba lance between them might play important roles in developing HAPE.