Perinatal hypoxia results in neuronal and endothelial cell damage. The main purpose of this study was to investigate the correlation of soluble intercellular adhesion molecule 1 (sICAM-1) expression and peripheral blood changes in perinatal asphyxia with neuronal injury markers in low birth weight (LBW) neonates. We compared the concentrations of serum sICAM-1, neuron-specific enolase (NSE) and antibodies specific for NR2 glutamate receptors in 29 asphyxiated and 20 control infants using standard enzyme immunoassay procedures. The mean total concentrations of sICAM-1 and neuron-specific proteins (NSE and NR2-specific antibodies) were higher in the asphyxiated infants than in the control infants. The serum sICAM-1 concentrations significantly correlated with Apgar scoring and with the pH and lactate data from capillary or arterial cord blood. No significant correlation between serum concentrations of neuron specific proteins and blood changes of asphyxia was found. Therefore, endothelial sICAM-1 expression levels might be accepted as an indicator of the severity of perinatal asphyxia in LBW infants.
Endothelial activity relects the balance of endogenous factors regulating vasoconstriction and vasodilation. Among these factors, nitric oxide (NO) is the most important contributor to the acute regulation of vascular tone. Altered nitric oxide synthesis by the vascular endothelium plays several important roles in the pathogenesis of neonatal disease through its efects on vascular homeostasis. However, the role of NO in the pathogenesis of perinatal brain injury has not been fully investigated. The present chapter explores how NO synthesis is regulated under physiological and pathological conditions, the impact of acute and chronic hypoxia on NO synthase activity in the vascular endothelium, and the role of perinatal endothelial dysfunction in the pathogenesis of neurodevelopmental disorders later in life.
Endothelial function plays an important role in the extrauterine adaptation of newborn infants. Endothelium produces different biologically active mediators, which play the central role in physiological and pathological processes and also in the extrauterine adaptation of newborn infants. The imbalance between vasoconstrictive and vasodilatation factors results in impaired cardiovascular adaptation and microcirculation and also brain injury. Microcirculatory disturbances are observed very often in preterm babies, who have a serious risk for perinatal brain injury and further neurodevelopment disabilities. Present chapter presents the pathogenetic role of vascular tone regulators of endothelial genesis in the formation of microcirculatory changes in preterm babies with a high risk of perinatal hypoxic encephalopathy.
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