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Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and Department of Pediatrics, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157
Our purpose was to determine
whether production of arachidonic acid metabolites, particularly
cyclooxygenase (COX) metabolites, is 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 analog, or the thromboxane mimetic
U46619. Radioimmunoassay was used to determine pulmonary artery
production of thromboxane B2 (TxB2) and
6-keto-prostaglandin F1
(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, whereas 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 toward constrictors, may
contribute to the early phase of chronic hypoxia-induced pulmonary
hypertension in newborn piglets.
cyclooxygenase-1; cyclooxygenase-2; prostacyclin; thromboxane
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