Carpenter T C, Reeves J T, Durmowicz A G
Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
J Appl Physiol (1985). 1998 Mar;84(3):1048-54. doi: 10.1152/jappl.1998.84.3.1048.
Recent clinical observations of a high incidence of preexisting respiratory infections in pediatric cases of high-altitude pulmonary edema prompted us to ask whether such infections would increase the susceptibility to hypoxia-induced pulmonary edema in young rats. We infected weanling rats with Sendai virus, thus causing a mild respiratory infection. Within 7 days of infection, Sendai virus was essentially undetectable by using viral culture and immunohistochemical techniques. Animals at day 7 of Sendai virus infection were then exposed to normobaric hypoxia (fraction of inspired O2 = 0.1) for 24 h and examined for increases in gravimetric lung water and in vascular permeability, as well as for histological evidence of increased lung water. Bronchoalveolar lavage was performed on a separate series of animals. Compared with control groups, infected hypoxic animals showed significant increases in perivascular cuffing, gravimetric lung water, and lung protein leak. In addition, infected hypoxic animals had increases in lavage fluid cell counts and protein content compared with controls. We conclude that young rats, exposed to moderate hypoxia while recovering from a mild viral respiratory infection, may demonstrate evidence of early pulmonary edema formation, a finding of potential relevance to human high-altitude pulmonary edema.
近期对小儿高原肺水肿病例中既往存在呼吸道感染高发病率的临床观察促使我们思考,此类感染是否会增加幼鼠对低氧诱导的肺水肿的易感性。我们用仙台病毒感染断奶幼鼠,从而引发轻度呼吸道感染。感染后7天内,通过病毒培养和免疫组化技术基本检测不到仙台病毒。然后,将感染仙台病毒7天的动物置于常压低氧环境(吸入氧分数=0.1)中24小时,并检测肺湿重和血管通透性的增加情况,以及肺含水量增加的组织学证据。对另一组动物进行支气管肺泡灌洗。与对照组相比,感染低氧动物的血管周围套袖现象、肺湿重和肺蛋白渗漏显著增加。此外,与对照组相比,感染低氧动物的灌洗液细胞计数和蛋白含量增加。我们得出结论,幼鼠在从轻度病毒性呼吸道感染中恢复的同时暴露于中度低氧环境,可能会出现早期肺水肿形成的证据,这一发现可能与人类高原肺水肿相关。