ABSTRACT
OBJECTIVES@#To study the effect of glucose metabolism disorders on the short-term prognosis in neonates with asphyxia.@*METHODS@#A retrospective analysis was performed on the medical data of the neonates with asphyxia who were admitted to 52 hospitals in Hubei Province of China from January to December, 2018 and had blood glucose data within 12 hours after birth. Their blood glucose data at 1, 2, 6, and 12 hours after birth (with an allowable time error of 0.5 hour) were recorded. According to the presence or absence of brain injury and/or death during hospitalization, the neonates were divided into a poor prognosis group with 693 neonates and a good prognosis group with 779 neonates. The two groups were compared in the incidence of glucose metabolism disorders within 12 hours after birth and short-term prognosis.@*RESULTS@#Compared with the good prognosis group, the poor prognosis group had a significantly higher proportion of neonates from secondary hospitals (48.5% vs 42.6%, @*CONCLUSIONS@#Recurrent hyperglycemia in neonates with asphyxia may suggest poor short-term prognosis, and it is necessary to strengthen the early monitoring and management of the nervous system in such neonates.
Subject(s)
Humans , Infant, Newborn , Asphyxia , Asphyxia Neonatorum/epidemiology , Hyperglycemia , Prognosis , Retrospective StudiesABSTRACT
AIM: To investigate whether oxytocin has neuroprotective effects on hippocampal CA 1 pyramidal neurons from neonatal rats exposed to hypoxic-ischemic brain injury and the underlying mechanisms.METHODS:An in vitro model of hypoxic-ischemic injury was used by exposing the brain slices to oxygen-glucose deprivation(OGD)solution. Acute dissociated brain slices(6~8 slices per rat)from 8 Sprague-Dawely rats of 7~10 d old were used.The slices were randomly divided into 4 groups: control group, OGD 20 min group, OGD 40 min group and OGD +oxytocin group.The effect of oxytocin on neuronal death was evaluated by TO-PRO-3 staining.Fresh brain slices from other 20 neonatal rats were divided into OGD group,OGD+oxytocin group,OGD+dVOT(oxytocin receptor antagonist)+oxytocin group,and OGD+bicucuclline(GABAAreceptor antagonist)+oxytocin group.The onset of anoxic depolarization in the hippocampal neurons treated with different drugs was recorded by whole-cell patch-clamp techniques.RESULTS: The results of TO-PRO-3 staining showed that neuronal deaths in hippocampal CA 1 area were increased over the prolonged OGD time.Oxyto-cin significantly reduced the hypoxic-ischemic deaths.Oxytocin dramatically prolonged the onset time of anoxic depolariza-tion after the application of OGD solution.Both dVOT and bicuculline blocked this effect.CONCLUSION: Oxytocin plays a neuroprotective role in neonatal rat hippocampal CA 1 pyramidal neurons by enhancing the inhibitory synaptic trans-mission via oxytocin receptors.Therefore,oxytocin is useful as a candidate for neuroprotective treatment after neonatal hy -poxic-ischemic brain injury.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the rebound depolarization of substantia gelatinosa (SG) neurons in rat spinal dorsal horn and explore its modulatory mechanisms to provide better insights into rebound depolarization-related diseases.</p><p><b>METHODS</b>Parasagittal slices of the spinal cord were prepared from 3- to 5-week-old Sprague-Dawley rats. The electrophysiologic characteristics and responses to hyperpolarization stimulation were recorded using whole-cell patch-clamp technique. The effects of hyperpolarization-activated cyclic nucleotide gated cation (HCN) channel blockers and T-type calcium channel blockers on rebound depolarization of the neurons were studied.</p><p><b>RESULTS</b>A total of 63 SG neurons were recorded. Among them, 23 neurons showed no rebound depolarization, 19 neurons showed rebound depolarization without spikes, and 21 neurons showed rebound depolarization with spikes. The action potential thresholds of the neurons without rebound depolarization were significantly higher than those of the neurons with rebound depolarization and spikes (-28.7∓1.6 mV vs -36.0∓2.0 mV, P<0.05). The two HCN channel blockers CsCl and ZD7288 significantly delayed the latency of rebound depolarization with spike from 45.9∓11.6 ms to 121.6∓51.3 ms (P<0.05) and from 36.2∓10.3 ms to 73.6∓13.6 ms (P<0.05), respectively. ZD7288 also significantly prolonged the latency of rebound depolarization without spike from 71.9∓35.1 ms to 267.0∓68.8 ms (P<0.05). The T-type calcium channel blockers NiCl2 and mibefradil strongly decreased the amplitude of rebound depolarization with spike from 19.9∓6.3 mV to 9.5∓4.5 mV (P<0.05) and from 26.1∓9.4 mV to 15.5∓5.0 mV (P<0.05), respectively. Mibefradil also significantly decreased the amplitude of rebound depolarization without spike from 14.3∓3.0 mV to 7.9∓2.0 mV (P<0.05).</p><p><b>CONCLUSION</b>Nearly two-thirds of the SG neurons have rebound depolarizations modulated by HCN channel and T-type calcium channel.</p>