Laboratory criteria of perinatal damage of central nervous system at premature newborns.

INTRODUCTION

Fetal and neonatal hypoxia takes a special place among the damaging factors of central nervous system (CNS). All forms of oxygen deficiency are accompanied by the development of bioenergetic hypoxia, which leads to tension of metabolic processes of the organism. Metabolic effect of hypoxia includes stark reduce of mitochondrial activity due to a significant inhibition enzymes of the Krebs cycle: succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH). In newborn babies is not always possible to objectively assess the condition of the CNS defeat, because very often the severity of lesions does not correspond to clinical symptoms, especially in premature newborns. So far determination the severity of hypoxic-ischemic CNS lesions is still very actual in modern medicine. More objective method of such an assessment is determine the activity of neurospecific enolase (NSE). The aim of the paper is to increase the efficiency of diagnosis of hypoxic CNS lesions in premature infants by determining the activity of NSE and study energy supply during the neonatal period.

MATERIAL AND METHODS

The concentration of NSE, SDH and LDH were determined in 15 conventionally healthy preterm infants (CHPI), which made the comparison group, and 64 premature babies with hypoxic-ischemic CNS lesions, which were divided into three groups: I group – 26 premature children with mild CNS lesions; II group – 20 premature children with severe hypoxic lesions and low birth weight; III group – 18 premature newborns with severe damage of central nervous system and extremely low birth weight. NSE activity was determined by enzyme immunoassay using reagents of the company «Fujirebio» (Sweden) on an automatic analyzer «Multiscan Plus» company «Labsystems» (Finland). Material for investigation was peripheral venous blood of newborns, which collected by vein punction at morning on an empty stomach.

RESULTS AND CONCLUSIONS

Metabolic effect of hypoxia in premature infants manifested by severe inhibition of mitochondrial respiratory activity, which appears in the reduction of aerobic enzyme activity of SDH and activation serum LDH. During the neonatal period in infants with perinatal hypoxic- ischemic lesions of the CNS levels of the of NSE, SDH and LDG aren’t normalized, that indicated on energy deficiency and requires the development of effective methods of correcting this condition. Perinatal hypoxia in premature neonates causes significant alteration of neuronal membranes and increase concentration in blood such neurospecific protein as NSE, whose concentration correlates with the degree of severity of CNS injury.