Fetal O2 changes in response to hypoxic stress: a mathematical model.
We developed a mathematical model to compute the time course of PO2 changes in fetal blood vessels during hypoxia. The model represents the circulation and major organs as a system of paths and nodes. We calculated outflow O2 for a path from its inflow O2 content and its distribution of transit times. The O2 content at a given node equals the flow-weighted sum of O2 delivered by different paths. Placental O2 transfer and organ O2 consumption are related to their arterial PO2 levels. We simulated the effects of uterine contractions with Gaussian-shaped decreases in placental O2 transfer. Increasing the intensity and increasing the duration of hypoxic episodes have comparable effects. Liver O2 consumption decreases more than that of other organs during hypoxic episodes. At the peak of a contraction, fetal systemic PO2 values decrease only about one-fourth as much as those in end-capillary placental blood. This indicates that despite rapid circulation times, fetal O2 reserves protect it against severe, short term hypoxia.
D001921:Brain / Q000098:blood supply / Q000378:metabolism; D003326:Coronary Circulation; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D005311:Fetal Hypoxia / Q000097:blood*; D006801:Humans; D000860:Hypoxia / Q000097:blood; D007668:Kidney / Q000098:blood supply / Q000378:metabolism; D008099:Liver / Q000098:blood supply / Q000378:metabolism; D008954:Models, Biological; D009206:Myocardium / Q000378:metabolism; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption; D010920:Placenta / Q000098:blood supply / Q000378:metabolism; D011247:Pregnancy; D014590:Uterine Contraction
D010100:Oxygen