In the mammalian fetus, the cardiovascular responses to acute hypoxaemia include a redistribution of the cardiac output away from the periphery towards the adrenal, myocardial and cerebral circulations. A component of the peripheral vasoconstriction is mediated by increased release of catecholamines into the fetal circulation during acute hypoxaemia. Previously, we have shown that the chick embryo also shows an increase in peripheral vascular resistance during acute hypoxaemia and that this response becomes progressively larger towards the end of the incubation period. However, the ontogeny of the catecholaminergic response to acute hypoxaemia has not been investigated in this species. Fertilised chicken eggs were studied on days 10, 13, 16 and 19 of incubation (hatching is at 21 days). At each stage of incubation, blood samples were obtained from the chorioallantoic artery of the chick embryos during normoxia and after 5 min of hypoxaemia for measurement of plasma concentrations of adrenaline and noradrenaline by HPLC. Basal plasma adrenaline and noradrenaline concentrations by the end of the incubation period were much higher in the chick embryo than values reported for mammalian fetuses during late gestation. During normoxia, basal plasma noradrenaline concentration remained unchanged during development but plasma adrenaline concentration showed a developmental increase from < 25.1 pmol l−1 at day 10 to 3 nmol l−1 at day 19 of incubation. Acute hypoxaemia caused an increase in plasma noradrenaline and adrenaline from day 13 and day 16 of incubation, respectively. In addition, the increase in plasma adrenaline and noradrenaline and in the ratio of plasma adrenaline to noradrenaline during acute hypoxaemia became progressively larger by the end of the incubation period. These data show an ontogenic increase in basal plasma catecholamines and in the catecholaminergic response to acute hypoxaemia in the chick embryo during the last third of the incubation period.

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1. Hyperoxia can cause local vasoconstriction in adult animal organs as a protective mechanism against hyperoxia-induced toxicity. It is not known at what time during development this vasoconstrictor capacity is present. Therefore, we measured the cardiac output (CO) distribution in different organs during a period of acute hyperoxia (100% Oµ) in the developing chick embryo. 2. Fertile eggs were divided into five incubation time groups (10 and 11, 12 and 13, 14 and 15, 16 and 17, and 18 and 19 days of a normal incubation time of 21 days). Eggs were opened at the air cell and a catheter was inserted into a branch of the chorioallantoic vein for injections of 15 ìm fluorescent microspheres during normoxia and at the end of 5 min (test group 1; n = 39) or 20 min (test group 2; n = 21) of hyperoxia exposure (100% Oµ). The fraction of CO to an organ was calculated as the fluorescence of the organ sample divided by the sum of the fluorescence of all organs. 3. Only in 18-and 19-day-old embryos did hyperoxia cause a decrease in the fractions of CO to the heart and carcass, and an increase in those to the yolk-sac and chorioallantoic membrane. This response was more pronounced after 20 min (test group 2) than after 5 min (test group 1) of hyperoxia with an additional decrease in the fractions of CO to the brain, intestine and liver (test group 2). 4. These data indicate that local mechanisms for hyperoxia-induced vasoconstriction in the heart, brain, liver, intestine and carcass develop late, during the final 15% of the incubation period, in the developing chick embryo. Keywords:

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