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As stated above, due to ethical and technical constraints, little is known about normal physiological values of CBF in healthy term neonates. Using Doppler sonography, Fenton et?al. measured cerebral blood flow velocity (CBFV) in the anterior and middle cerebral arteries of 128 healthy term neonates during the first week of postnatal life [50]. They have found an important decrease in cerebrovascular resistance during the first 24?h following birth, and this was accompanied by a nearly B3GAT3 twofold gradual increase in CBFV through the first 4?days of postnatal life. Reporting mean CBF values does not reflect the important amount of interindividual variability of CBF being present even in within a relatively homogenous patient population. In a consecutive series of 25 mechanically ventilated neonates, CBF varied between 4.3 and 18.9?ml/100?g��min?1 [51]. This huge interindividual variability is further emphasized by positron emission tomography measurements, where CBF varied between 9 and 73?ml/100?g��min?1 in 14 term neonates, and between 4.9 and 23?ml/100?g��min?1 in 16 preterm infants [52]. Of utmost interest, all infants in this study those had CBF values inferior to 10?ml/100?g��min?1 in the early postnatal period appeared normal at subsequent neurological examinations [52]. These observations thus suggest that, in contrast to adults [46], even very low CBF levels in the early postnatal period might be sufficient to maintain CNS function, at least in certain patients. In line with this hypothesis, a combination of Xe-133 measurement of CBF together with amplitude-integrated electroencephalogram in 20 mechanically ventilated preterm infants selleck compound (27�C33?w) during the first 48?h following birth revealed the presence of cortical electrical activity at flow rates as low as 3?ml/100?g��min?1 [53]. Also, measurements of visual evoked potentials in 32 premature neonates of AUY-922 in vitro 5?kPa [54]. The fact that cerebral functions may persist at even very low CBF in infants does not, however, mean that low cerebral flow can harmlessly supported in this patient population in general. Indeed, although it is ethically unacceptable to conduct such studies, the high interindividual variability in CBF may imply that a given individual with relatively high CBF values at rest might not tolerate low CBF rates. The majority of studies addressing CBF in the neonate measured global flow. As the preterm infant is at high risk of white matter injury, and ischemia is considered as the major cause to induce this morbidity, an important question is whether CBF is quantitatively comparable between the cerebral gray and white matter. Only few works investigated this question in neonatal populations.
