AbstractExposure of chick embryos to moderate hypoxia (6–10% O2for 4–6 hours) induces a marked blood‐volume increase. This treatment also precipitates hemorrhage that can cause death or malformation or both when localized near rapidly developing structures. To determine whether the hypoxia‐induced hypervolemia can raise embryonic blood pressure to a hemorrhage level, the mean ventricular blood pressure (MVBP) of 587 embryos was measured before, during, and after treatment. The mean MVBP of 3‐day embryos rose from 11.1 mm water to 14.7 mm during the first two hours of hypoxia, dropped slowly during the rest of treatment, then increased again after exposure to air. The highest mean values (16.4 mm) were obtained two hours after treatment, coinciding with the time of maximum hemorrhage. The range of MVBP at that time was wide (6.0–27.0 mm) and in many embryos was twice as high as normal. The MVBP gradually returned to normal 2–13 hours after treatment. Maximum increases in the MVBP of 4 to 5‐day embryos also occurred during the second hour after treatment, but recovery after that was faster than at three days.In a parallel experiment hypervolemia was induced by sequential injection of saline into the ventricles of 3‐day embryos, in between pressure measurements. The MVBP rose slowly up to 30 mm water. Bleeding usually began at pressures of 18 mm. Hypervolemia induced by hypoxia appears to be responsible for the blood‐pressure increases and the development of teratogenically i