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Articles in PresS, published online ahead of print November 8, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00246.2002
Submitted on July 25, 2002
Accepted on November 4, 2002
1 Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA
2 Department of Pediatrics, University of New Mexico School of Medicine, Albuquerque, NM, USA
3 Department of Pediatrics, Wake Forest University School of Medicine, Winston-Salem, NC, USA
* To whom correspondence should be addressed. E-mail: cfike{at}wfubmc.edu.
Altered NO production could contribute to the pathogenesis of hypoxia-induced pulmonary hypertension. To determine whether parameters of lung NO are altered at an early stage of hypoxia-induced pulmonary hypertension, newborn piglets were exposed to room air (control, n=21), or 10% O2 (hypoxia, n=19) for 3-4 days. Some lungs were isolated and perfused for measurement of exhaled NO output and the perfusate accumulation of nitrite and nitrate (NOx-), the stable metabolites of NO. Pulmonary arteries (PA, 20-600 µm diameter) and their accompanying airways were dissected from other lungs and incubated for NOx- determination. Abundances of the NOS isoforms, eNOS and nNOS, were assessed in homogenates of PAs and airways. The perfusate NOx- accumulation was similar whereas exhaled NO output was lower for isolated lungs of hypoxic as compared to control piglets. The incubation solution NOx- did not differ between PAs of the two groups but was lower for airways of hypoxic as compared to control piglets. Abundances of both eNOS and nNOS proteins were similar for SPA homogenates from the two groups of piglets but were increased in airway homogenates of hypoxic as compared to controls. The NO pathway is altered in airways but not in PAs at an early stage of hypoxia induced pulmonary hypertension in newborn piglets.
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