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Articles in PresS, published online ahead of print September 27, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00228.2002
Submitted on July 15, 2002
Accepted on September 24, 2002
1 Department of Pediatrics, Wake Forest University School of Medicine, Winston-Salem, NC, USA
2 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: cfike{at}wfubmc.edu.
Our purpose was to determine if production of arachidonic acid metabolites, particularly cyclooxygenase (COX) metabolites, are altered in 100-400 µm diameter pulmonary arteries of piglets at an early stage of pulmonary hypertension. Piglets were raised in either room air (control) or hypoxia for 3 days. A cannulated artery technique was used to measure responses of 100-400 µm diameter pulmonary arteries to arachidonic acid, a prostacyclin analogue, or the thromboxane mimetic, U46619. Radioimmunoassay was used to determine pulmonary artery production of TXB2 and 6-keto PGF1
, the stable metabolites of thromboxane and prostacyclin, respectively. Assessment of abundances of COX pathway enzymes in pulmonary arteries was determined by immunoblot technique. Arachidonic acid induced less dilation in pulmonary arteries from hypoxic than in pulmonary arteries from control piglets. Pulmonary artery responses to prostacyclin and U46619 were similar for both groups. 6-keto PGF1 production was reduced; whereas TXB2 production was increased in pulmonary arteries from hypoxic piglets. Abundances of both COX 1 and prostacyclin synthase were reduced; while abundances of both COX 2 and thromboxane synthase were unaltered in pulmonary arteries from hypoxic piglets. At least partly due to altered abundances of COX pathway enzymes, a shift in production of arachidonic acid metabolites, away from dilators towards constrictors, may contribute to the early phase of chronic hypoxia-induced pulmonary hypertension in newborn piglets.
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