Control of cerebral circulation in the high‐risk Neonate

Abstract

A knowledge of neonatal cerebrovascular physiology is essential to the understanding of diseases that frequently affect the subsequent development of the newborn brain. Recent observations indicate that the cerebral vessels of the healthy newborn infant, even the very preterm, respond to physiological stimuli in the same manner as in the mature organism. Thus, cerebral blood flow changes with changes in arterial carbon dioxide tension (PaCO2), oxygen concentration (CaO2), or glucose concentration, whereas cerebral blood flow remains constant at minor fluctuations in arterial blood pressure. In pathological states, pressure autoregulation may become impaired, and in severe cases the vessels do not react to chemical or metabolic stimuli. These infants are at high risk for developing cerebral lesion, and they may be candidates for new "brain-protecting regimens."

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

“…The sheep fetus displays cerebral hemodynamics similar to humans and permits repeated physiological measurements in utero in the unanesthetized state. Importantly, similar to the human fetus [77][78][79][80], the fetal sheep displays a very limited range of cerebral autoregulation under normal conditions and a pressure-passive cerebral circulation when subjected to systemic hypoxia and associated hypotension [66,[81][82][83][84]. Moreover, measurements of BP, electroencephalography, blood oxygenation, and other vital variables can be correlated with acute changes in cerebral blood flow and metabolism.…”

Sonographic Changes in Hypoxic-Ischaemic Encephalopathy

“…BFV has been recorded higher in infants with permanent brain damage during the first days of life (Pryds, 1991;Ilves et al, a, 2009b. Severe increase in cerebral BFV and the decrease in RI take place in asphyxiated infants with severe HIE and a poor prognosis by the second half of the first day, being most severe during the first 3 days (Bennhagen et al, 1998;Ilves et al, 2009a;Meek et al, 1999;Pryds et al, 1990).…”

“…The major regulatory mechanism for the cerebral blood flow is autoregulation (Pryds et al, 1990(Pryds et al, , 1991, but also PaCO2, the oxygen and blood glucose delivery and the total haemoglobin concentration level (Volpe, 2005).…”

“…In this situation, dissociation exists between the cerebral metabolic rate and the over-abundant BFV relative to the metabolic needs of the brain tissue, the socalled luxury perfusion (Levene et al, 1989). Markedly high BFV despite isoelelctric EEG activity is found in these infants (Pryds, 1991). The BFV was higher, but the cross-brain oxygen extraction was lower in asphyxiated infants who died, compared to the neonates who survived with a normal neurologic outcome (Frewen et al, 1991).…”

“…The mechanism of such luxury cerebral perfusion following ischaemic brain injury is still unclear. The neuronal disruption causing release of vasoactive substances such as adenosine and lactate, or of excitatory amino acids (Pryds, 1991), irreversible cerebral vascular injury with a complete loss of tone in resistance vessels may play a role in the pathogenesis of delayed hyperaemia (Fellman & Raivio, 1997;Levene et al, 1989;Pryds et al, 1990).…”