Oxygen affinity of haemoglobin modulates cerebral blood flow in premature infants. A study with the non-invasive xenon-133 method

Abstract

Low cerebral blood flow (CBF) is thought to cause ischaemic brain lesions in premature infants, but a normal outcome has also been observed. Low oxygen affinity of haemoglobin and high arterial oxygen content, independently, reduce CBF under normal, physiological conditions. Transfusions lower the amount of fetal haemoglobin [HbF] and therefore the oxygen affinity of premature babies. In 47 premature babies (range of gestational age 25-34 weeks, birthweight 740-1370 g), CBF was measured with the i.v. Xenon 133 method on days 1, 3 and 7. The relative amount of fetal haemoglobin [HbF] was used as a marker of oxygen affinity of haemoglobin and the haematocrit as representing the arterial oxygen content. A significant influence of [HbF] on CBF was found on days 1, 3 and 7 in ultrasonographically normal babies (n = 13). In babies with subependymal and/or intraventricular haemorrhage (n = 15), this correlation was significant only on day 3 and in those with abnormal intraparenchymal echodensities (n = 19) only on day 7. The correlation between haemoglobin concentration and CBF was not significant. Multiple regression analysis showed a significant influence of [HbF] on CBF independent of haematocrit, pCO2 and blood pressure. It appears that, after blood transfusion, normal babies, and to a lesser extent those with haemorrhages are able to lower their CBF according to the actual oxygen affinity of blood. However, low CBF (less than 10 ml/100 g/min) in non-transfused babies was often associated with later development of cystic periventricular leukomalacia.)