Effects of prenatal hypoxia on pulmonary vascular reactivity in chickens prone to pulmonary hypertension.
Among chickens, meat-producing broiler strains are highly prone to develop severe pulmonary hypertension (PH) that is accompanied by endothelial dysfunction in the conduit extrapulmonary arteries. We hypothesized that exposure to chronic prenatal mild hypoxia would accelerate PH and endothelial dysfunction in smaller intrapulmonary arteries from broiler chickens. Fertilized broiler and layer (White Leghorn, WL) eggs were incubated under normoxic or hypoxic conditions. Endothelium-dependent (tested with acetylcholine, ACh ) and -independent (tested with sodium nitroprusside, SNP) relaxations of the caudomedial intrapulmonary artery were studied on fetal day 19 and at 2 weeks post-hatch. The response to acute hypoxia in vitro was also studied in the 2 wk-old vessels. Relaxations induced by ACh and SNP were similar in broiler and layer chickens and were unaffected by chronic mild hypoxia during incubation. However, during in vitro acute hypoxia the broiler arteries showed a markedly enhanced contraction. Chronic prenatal hypoxia did not affect the response of intrapulmonary arteries to acute hypoxia. We conclude that early endothelial dysfunction is not present in the small pulmonary arteries of fast-growing broilers after incubation under normoxic or hypoxic conditions. The higher susceptibility of the broiler pulmonary arteries to acute hypoxia might, at least partially, explain the higher susceptibility to PH.
Department of Pediatrics, Maastricht University Medical Center, School for Oncology and Developmental Biology, P. Debyelaan 25, University of Maastricht, Maastricht, The Netherlands.
B
B
Zoer
L
L
Kessels
A
A
Vereijken
J G R
JG
De Mey
V
V
Bruggeman
E
E
Decuypere
C E
CE
Blanco
E
E
Villamor
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002642:Chick Embryo; D002645:Chickens; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D006976:Hypertension, Pulmonary / Q000209:etiology* / Q000503:physiopathology; D000860:Hypoxia; D009599:Nitroprusside / Q000494:pharmacology; D011651:Pulmonary Artery / Q000187:drug effects / Q000378:metabolism*; D014661:Vasoconstriction; D014664:Vasodilation / Q000187:drug effects
D009599:Nitroprusside; D000109:Acetylcholine