title: Chronic moderate hypoxia during in ovo development alters arterial reactivity in chickens.
abstract: We previously observed arterial sympathetic hyperinnervation and endothelial dysfunction in the chicken embryo after exposure to chronic hypoxia. We now investigate whether changes in arterial properties could also be observed at 14-15 weeks of life. Eggs of White Leghorn chicken were incubated under normoxic or moderately hypoxic (15% O2 from days 6-19 of a 21-day incubation) conditions. Experiments were performed at 14-15 weeks of life under standard conditions (Hm: males exposed to hypoxia; Hf: females exposed to hypoxia; Nm: males exposed to normoxia; Nf: females exposed to normoxia). Body weight at hatching and at 14-15 weeks was not affected by in ovo exposure to hypoxia. Mean arterial pressure and heart rate were not significantly altered by chronic in ovo hypoxia. However, isolated femoral arteries were more sensitive to electrical stimulation (frequency in Hz of half-maximal contraction, Hm: 1.62+/-0.33, Hf: 1.92+/-0.88, Nm: 2.49+/-0.49, Nf: 2.83+/-0.31) and pharmacological stimulation of peri-arterial sympathetic nerves (contraction in N/m in response to tyramine: Hm: 5.27+/-0.85, Hf: 4.10+/-0.9, Nm: 2.26+/-0.67, Nf: 3.65+/-0.51, p=0.07) after in ovo hypoxia. In side branches of the femoral artery, the effect of NO synthase blockade with L-NAME on contraction (in N/m) in response to high K+ (Hm: 0.35+/-0.91, Hf: 1.29+/-0.36, Nm: 2.88+/-0.19, Nf: 2.79+/-0.58) and on the sensitivity to acetylcholine (DeltapD2, H: 0.32+/-0.11, N: 0.62+/-0.05) was reduced after in ovo hypoxia. The present study shows that exposure to chronic moderate hypoxia during development affects the contractile and relaxing arterial responses of 14- to 15-week-old chickens. Although hypoxia did not lead to changes in blood pressure at this age, the observed effects on arterial sympathetic and endothelial function may represent early signs of future cardiovascular abnormalities.
authors.affiliation: Department of Pediatrics, Research Institute Growth and Development (GROW), University Hospital Maastricht, Maastricht, The Netherlands.
authors.forename: K
authors.initials: K
authors.lastname: Ruijtenbeek
authors.forename: C G A
authors.initials: CG
authors.lastname: Kessels
authors.forename: B J A
authors.initials: BJ
authors.lastname: Janssen
authors.forename: N J J E
authors.initials: NJ
authors.lastname: Bitsch
authors.forename: G E
authors.initials: GE
authors.lastname: Fazzi
authors.forename: G M J
authors.initials: GM
authors.lastname: Janssen
authors.forename: J
authors.initials: J
authors.lastname: De Mey
authors.forename: C E
authors.initials: CE
authors.lastname: Blanco
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000097:blood / Q000254:growth & development; D001794:Blood Pressure; D001835:Body Weight; D002642:Chick Embryo; D002908:Chronic Disease; D003345:Corticosterone / Q000097:blood; D005260:Female; D005263:Femoral Artery / Q000503:physiopathology; D006339:Heart Rate; D000860:Hypoxia / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D003345:Corticosterone; D009638:Norepinephrine