Schoene R B, Goldberg S
Colorado Altitude Research Institute, Keystone 80435.
Int J Sports Med. 1992 Oct;13 Suppl 1:S59-61. doi: 10.1055/s-2007-1024595.
The understanding of the mechanisms underlying certain human diseases usually requires an animal model which can be manipulated in a way that will allow dissection of the pathophysiologic events which lead to the disease. High altitude pulmonary edema (HAPE) occurs in some healthy individuals who ascend from low to high altitude. The disease is characterized by a high protein leak into the lungs and is associated with accentuated pulmonary hypertension. Attempts to find an animal model for HAPE have been made in a number of animal species, including rats, rabbits, sheep, dogs and ferrets. None has been consistently successful. Utilizing the physiologic characteristic of an accentuated hypoxic pulmonary vascular response, we studied both pigs and rats during the stresses of hypoxia and exercise (rats) and examined the lungs for the cellular, protein, and morphologic changes. Protein and cell contents in the lung lavage of the hypoxic animals were slightly higher than the controls while the presence of von Willebrand factor in the hypoxic animals suggests early epithelial damage. This presentation will review previous attempts to find an animal model of HAPE and will discuss the preliminary results of our studies with their suggestive but not confirmatory results.
对某些人类疾病潜在机制的理解通常需要一个动物模型，该模型能够以某种方式进行操控，以便剖析导致疾病的病理生理事件。一些从低海拔升至高海拔的健康个体中会发生高原肺水肿（HAPE）。该疾病的特征是高蛋白渗漏到肺部，并伴有肺动脉高压加剧。人们已在包括大鼠、兔子、绵羊、狗和雪貂在内的多种动物物种中尝试寻找HAPE的动物模型，但均未一直成功。利用缺氧性肺血管反应加剧的生理特征，我们在缺氧和运动应激（针对大鼠）过程中对猪和大鼠进行了研究，并检查了肺部的细胞、蛋白质和形态学变化。缺氧动物肺灌洗中的蛋白质和细胞含量略高于对照组，而缺氧动物中血管性血友病因子的存在表明早期上皮损伤。本报告将回顾此前寻找HAPE动物模型的尝试，并讨论我们研究的初步结果，这些结果具有提示性但不具有确定性。
