Introduction During hypoxia the chick embryo shows a redistribution of the cardiac output similar to the mammalian fetus, favoring vital organs like the heart and brain. The redistribution of the cardiac output results from peripheral vasoconstriction or vasodilatation in different circulations. The present study examined the role of nitric oxide on the vasodilatator responses during hypoxia in the chick embryo.

Method 60 Fertilized eggs from day 11 to 19 of incubation (of 21 days) were divided in 2 groups. The eggs were opened at the air cell and a chorio-allantoic vein was catheterized for injection of either nitric oxide synthase inhibitor L-NAME, or NaCl 0.9%. We waited 15 minutes before starting the experiment. Fluorescent microspheres were injected in normoxia, after 5 min. of hypoxia and after 5 min. of reoxygenation. After the injections the embryos were sacrificed and the different organs were dissected and digested for microsphere isolation and subsequent fluorescent analysis.

Results No difference was found in the cardiac output distribution in normoxia or hypoxia for both the L-NAME and NaCl group. After reoxygenation, the fraction of the cardiac output directed to the chorioallantoic membrane (placenta equivalent) increased, but not in the L-NAME treated group.

Conclusion In the chick embryo the redistribution of the cardiac output in response to hypoxia appears independent of nitric oxide-induced vasodilatation. In contrast, following reoxygenation the increase of the fraction of the cardiac output directed to the chorio-allantoic membrane has a NO component.