Background and aims Infants with intrauterine growth retardation are prone to intestinal dysfunction which is manifested by feeding intolerance and, in the most severe cases, necrotizing enterocolitis. The morphological and molecular mechanisms that lead to these complications are not completely understood and suitable experimental models are necessary. We aimed to characterize mesenteric artery (MA) reactivity, small intestine morphometry and intestinal expression of VEGF in a chicken model of hypoxia-induced fetal growth restriction.
Methods Chicken embryos (15 and 19 days) and hatchlings (< 3-h-old and 1-d-old) were incubated under hypoxic (15% O2 from day 0 to day 19 of incubation) or normoxic conditions. Vascular reactivity was studied using wire miography. Intestinal morphometry was assessed in hematoxyline-eosine-stained sections. The expression of VEGF mRNA was determined by RT-PCR analysis.
Results Hypoxia altered the responsiveness of chicken embryo MAs to acetylcholine, the NO donor sodium nitroprusside and the constrictor polypeptide ET-1. However, the majority of these alterations, with the exception of the hyperresponsiveness to ET-1, were not present in the hypoxic hatchlings. When intestinal histology was analyzed, subtle hypoxia-induced changes were noted in the muscularis propia and the villi from the hatchlings. Hypoxic incubation also diminished the expression of VEGF mRNA in the terminal ileum of the hatchlings.
Conclusions Chronic moderate hypoxia during incubation results in subtle but significant alterations in chicken MA reactivity, small intestine morphology and VEGF expression. Whether these alterations may have a direct effect on the functional status of the intestine remains to be investigated.