The dynamic changes of plasma neuropeptide y and neurotensin and their role in regulating cerebral hemodynamics in neonatal hypoxic-ischemic encephalopathy.

Hypoxic-ischemic encephalopathy (HIE) is a common cause of neonatal encephalopathy and is one of the most important causes of neonatal death and disabilities, especially those infants with moderate to severe encephalopathy. However, the pathogenesis of HIE still remains unclear. The purpose of this study was to explore the dynamic changes in plasma neuropeptide Y (NPY) and neurotensin (NT) as well as their role in regulating cerebral hemodynamics in HIE patients. The plasma levels of NPY and NT in the umbilical artery and peripheral blood on the first, third, and seventh days after birth in 40 term infants with HIE and 40 healthy controls were measured using radioimmunoassay. On the first day of life, the blood samples were collected immediately when ultrasound examinations were finished. The ultrasound transducer was placed on the temporal fontanelle to detect the hemodynamic parameters of the middle cerebral artery, including peak systolic flow velocity, end-diastolic flow velocity, time-average mean velocity, pulsatility index, and resistance index (RI) in both groups were measured by pulse Doppler ultrasound in the first day after birth. The relationship between RI and NPY or NT was analyzed by linear regression analysis. NPY levels in umbilical blood ([mean +/- standard deviation] 615.5 +/- 130.7 ng/L) and first-day peripheral blood (355.9 +/- 57.4 ng/L) in neonates with HIE were significantly higher than those in normal newborns' blood (199.1 +/- 63.2 and 214.4 +/- 58.0 ng/L, respectively; P < 0.01). NPY levels in HIE neonates then declined to control levels on the third day after birth ( P > 0.05). However, the levels of plasma NT in umbilical blood and peripheral blood were much higher in the HIE group than those in normal newborns during the first week ( P < 0.01). The results of Doppler ultrasound examinations showed that cerebral blood flow velocity significantly decreased, whereas RI increased markedly in HIE patients compared with healthy controls ( P < 0.01). Linear regression analysis revealed that the RI was positively correlated with NPY levels ( R = 0.614; P < 0.01) and negatively correlated with NT levels ( R = -0.579; P < 0.01). The results of this study showed that there was a significant increase in plasma NPY and NT levels in HIE patients and this was strongly related to the severity of HIE, and the hemodynamic parameter RI was significantly correlated with NPY and NT. Therefore, we believe that the dynamic changes in plasma NPY or NT levels participate in the mechanisms of HIE by regulating cerebral hemodynamic changes after neonatal asphyxia occurs.