VIRAL RESPIRATORY-INFECTION INCREASES SUSCEPTIBILITY OF YOUNG-RATS TOHYPOXIA-INDUCED PULMONARY-EDEMA

Recent clinical observations of a high incidence of preexisting respir atory infections in pediatric cases of high-altitude pulmonary edema p rompted us to ask whether such infections would increase the susceptib ility to hypoxia-induced pulmonary edema in young rats. We infected we anling rats with Sendai virus, thus causing a mild respiratory infecti on. Within 7 days of infection, Sendai virus was essentially undetecta ble by using viral culture and immunohistochemical techniques. Animals at day 7 of Sendai virus infection were then exposed to normobaric hy poxia (fraction of inspired O-2 = 0.1) for 24 h and examined for incre ases in gravimetric lung water and in vascular permeability, as well a s for histological evidence of increased lung water Bronchoalveolar la vage was performed on a separate series of animals. Compared with cont rol groups, infected hypoxic animals showed significant increases in p erivascular 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 y oung rats, exposed to moderate hypoxia while recovering from a mild vi ral respiratory infection, may demonstrate evidence of early pulmonary edema formation, a finding of potential relevance to human high-altit ude pulmonary edema.