Fetal response to intrauterine stress

Many human infants are born inappropriately small as a result of stress suffered during intrauterine life. Acute reductions in oxygen delivery to fetal tissues have therefore been studied in animals so that insight can be obtained into the adaptive mechanisms that underlie human developmental abnormalities. It is now known that during moderate hypoxic stress fetal arterial blood pressure is variably increased while heart rate and cardiac output are depressed; blood volume is reduced but cardiac output is redistributed to spare the myocardium, brain and adrenal glands at the expense of most other organs. Also a greater fraction of oxygen-rich venous blood from the placenta is returned to the heart for distribution. Spared organs are those that grow disproportionately well in human asymmetrical intrauterine growth retardation (IUGR). These cardiovascular responses are not fully understood although elevated fetal plasma levels of catecholamines and a host of fetal hormones are undoubtedly important. Chemical sympathectomy does not abolish the blood flow redistribution phenomenon, which implies that autoregulatory effects may be responsible for some of the redistribution of blood flow. Fetal hypoxaemia and metabolic abnormalities are sequelae often found with human IUGR, suggesting placental exchange defects. IUGR placentas appear to have defective transport mechanisms for many nutrients. Animal studies suggest that the placenta will give priority to its own needs over those of the fetus, when necessary, to support its own growth and function.