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Am J Physiol Lung Cell Mol Physiol 279: L547-L554, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 3, L547-L554, September 2000

Endothelin receptor blockade decreases lung water in young rats exposed to viral infection and hypoxia

Todd C. Carpenter and Kurt R. Stenmark

Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262

Viral respiratory infections may increase the susceptibility of young animals to hypoxia-induced pulmonary edema. Because hypoxia stimulates endothelin production, we hypothesized that an increase in lung endothelin contributes to these alterations in lung water. Weanling rats were infected with Sendai virus, causing a mild respiratory infection. At day 7 after infection, animals were exposed to hypoxia (inspired O2 fraction = 0.1) for 24 h. Exposure to virus plus hypoxia led to increases in lung water compared with control groups (P < 0.001). Lung endothelin levels were significantly higher in the virus plus hypoxia group than in control groups (P < 0.001). A second group of infected animals received bosentan, a nonselective endothelin receptor antagonist, during exposure to hypoxia. Bosentan-treated animals showed less lung water accumulation, less lung lavage fluid protein, and less perivascular fluid cuffing than untreated animals (P < 0.01). We conclude that the combination of a recent viral respiratory infection and exposure to moderate hypoxia led to increases in endothelin in the lungs of young rats and that endothelin receptor blockade ameliorates the hypoxia-induced increases in lung water found in these animals.

high-altitude pulmonary edema; Sendai virus; bosentan; preproendothelin


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