Acute hypoxia‐reoxygenation and vascular oxygen sensing in the chicken embryo

Fetal/perinatal hypoxia is one of the most common causes of perinatal morbidity and mortality and is frequently accompannied by vascular dysfunction. However, the mechanisms involved have not been fully delineated. We hypothesized that exposure to acute hypoxia‐reoxygenation induces alterations in vascular O(2) sensing/signaling as well as in endothelial function in the chicken embryo pulmonary artery (PA), mesenteric artery (MA), femoral artery (FA), and ductus arteriosus (DA). Noninternally pipped 19‐day embryos were exposed to 10% O(2) for 30 min followed by reoxygenation with 21% O(2) or 80% O(2). Another group was constantly maintained at 21% O(2) or at 21% O(2) for 30 min and then exposed to 80% O(2). Following treatment, responses of isolated blood vessels to hypoxia as well as endothelium‐dependent (acetylcholine) and ‐independent (sodium nitroprusside and forskolin) relaxation were investigated in a wire myograph. Hypoxia increased venous blood lactate from 2.03 ± 0.18 to 15.98 ± 0.73 mmol/L (P < 0.001) and reduced hatchability to 0%. However, ex vivo hypoxic contraction of PA and MA, hypoxic relaxation of FA, and normoxic contraction of DA were not significantly different in any of the experimental groups. Relaxations induced by acetylcholine, sodium nitroprusside, and forskolin in PA, MA, FA, and DA rings were also similar in the four groups. In conclusion, exposure to acute hypoxia‐reoxygenation did not affect vascular oxygen sensing or reactivity in the chicken embryo. This suggests that direct effects of acute hypoxia‐reoxygenation on vascular function does not play a role in the pathophysiology of hypoxic cardiovascular injury in the perinatal period.