Abstract
Background Among chickens, meat producing broiler strains are highly prone to develop severe pulmonary hypertension (PH) associated with endothelial dysfunction. However, pulmonary endothelial function appears to be unaffected during prenatal life.
Objective to test the hypothesis that exposure to chronic prenatal hypoxia induces endothelial impairment and accelerates the development of PH in chickens prone to the disease.
Methods Fertilized eggs from two genetic lines of broiler chickens differing in susceptibility to PH (high sensitivity: HS, low sensitivity: LS) were incubated under normoxic or hypoxic (15% O2) conditions from day 6 to day 19 of a 21-d incubation period. On day 19 isolated intrapulmonary artery segments were mounted in a myograph for isometric tension recording. The contractile responses induced by KCl as well as the relaxations induced by acethylcholine (ACh), the nitric oxide donor sodium nitroprusside (SNP), and the adenylate cyclase activator forskolin were tested.
Results Hypoxia produced a reduction in the weight of the HS (31.1 ± 0.6 g vs 27.3 ± 0.6 g, P<0,001) and the LS (32.1± 0.6 vs 28.6 ± 0.9 P<0,001) embryos. KCl-induced contraction was unaffected by hypoxia in both groups. Endothelium-dependent (induced by ACh) and -independent (induced by SNP and forskolin) relaxations were also unaffected by hypoxia in both groups. ACh-induced relaxation was reduced by the NO synthase inhibitor L-NAME (10 mM) and abolished by the soluble guanylyl cyclase inhibitor ODQ (10 microM). L-NAME induced inhibition of ACh-induced relaxation was less marked in normoxic embryos of the HS group than in the other three groups.
Conclusions Chronic hypoxia during incubation reduced embryonic growth but did not influence vascular reactivity in chicken embryos prone to postnatal pulmonary hypertension.
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Van Der Weerden, M., Agren, P., Kessels, C. et al. 388 Chonic Hypoxia did not Affect Pulmonary Vascular Reactivity in Chicken Embryos Prone to Pulmonary Hypertension. Pediatr Res 58, 421 (2005). https://doi.org/10.1203/00006450-200508000-00417
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DOI: https://doi.org/10.1203/00006450-200508000-00417