Hyperoxia and local organ blood flow in the developing chick embryo

1. Hyperoxia can cause local vasoconstriction in adult animal organs as a p rotective mechanism against hyperoxia-induced toxicity It is not known at w hat time during development this vasoconstrictor capacity is present. There fore, we measured the cardiac output (CO) distribution in different organs during a period of acute hyperoxia (100% O-2) in the developing chick embry o. 2. Fertile eggs were divided into five incubation time groups (10 and 11, 1 2 and 13, 14 and 15, 16 and 17, and 18 and 19 days of a normal incubation t ime of 21 days). Eggs were opened at the air cell and a catheter was insert ed into a branch of the chorioallantoic vein for injections of 15 mu m fluo rescent 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% O-2). The fraction of CO to an organ was calculated as the fluorescence of the o rgan 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 af ter 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 far hyperoxia-induced vasocons triction in the heart, brain, liver, intestine and carcass develop late, du ring the final 15% of the incubation period, in the developing chick embryo .