实验性高原肺水肿发病机制的初步研究

本研究用Ｗｉｓｔａｒ大鼠在模拟海拔６０００ｍ高度停留４８ｈ，对实验性高原肺水肿的发病机制进行了初步观察，结果表明：（１）大鼠肺血管外含水量明显增多；（２）肺泡隔增宽，肺泡隔内血管口径大小不一，有的扩张，有的狭窄甚至闭锁，硝酸镧示踪电镜术发现肺泡上皮、血管内皮和肺泡隔内有数量不等的镧颗粒；（３）硝苯啶或地塞米松均可使肺血管外含水量明显降低，二者联合作用效果更佳；（４）血浆内心钠素（ＡＮＰ）含量明显增多，伴有体重和血液含水量明显减少。从而表明，低氧性肺动脉压升高和肺泡壁微血管壁通透性增强在高原肺水肿的发生中有重要作用。血浆ＡＮＰ增加和伴随的血液浓缩是对抗血浆进一步外渗的因素之一。

A PRELIMINARY STUDY ON PATHOGENESIS OF EXPERIMENTAL HIGH ALTITUDE PULMONARY EDEMA

The pathogenesis of experimental high altitude pulmonary edema in rats were preliminary observed. The results indicated that after acute exposure to simulated altitude of 6 000m for 48 h the rats presented significant increase in pulmonary extravascular water volume (PEWV), severe interstitial edematous widening of alveolar septum, uneven changes (dilatation, constriction or even closure) of vascular diameter in alveolar septum and lanthanum granules in alveolar epithelium, septum and vascular endothelium by lanthanum nitrate (LaNO3) tracer electron micrography. Prophylactic administration of nifedipine or dexamethasone was effective in lowering PEWV and the effect was more powerful when they were used in combination. Atrial natriuretic peptide (ANP) content in plasma significantly increased while body weight and water contant in blood significantly diminished. The results suggest that hypoxia-induced increase in pulmonary artery pressure and pulmonary vascular permeability may play an important role in the occurrence of altitude pulmonary edema. Increase in ANP content in plasma and hemoconcentration may be beneficial for prevention of further increase in pulmonary extravascular water.