ABSTRACT
Objective To investigate the pathophysiological role of serum hydrogen sulfide (H2 S) and its correlation with serum neuron-specific enolase (NSE) level in the process of febrile seizures (FS).Methods Sixty-five children with FS and acute upper respiratory infection were selected as FS group,51 children with acute upper respiratory infection associated with fever were taken as upper respiratory infection group and 43 healthy children in Child Health Section for physical examination were respectively chosen as the healthy control group.All children came from Department of Pediatrics of Zhujiang Hospital,Southern Medical University from Mar.15 to Nov.10,2012.The serum H2S and NSE levels of all groups were measured by Microplate Reader.Results The serum H2S in FS group was significantly lower than that in upper respiratory infection group and healthy control group (all P ＜ 0.01) ; the NSE level in FS group was significantly higher than that in upper respiratory infection group and healthy control group (all P ＜0.01) ;the levels of H2S and NSE had no significant differences between upper respiratory infection group and healthy control group (all P ＞ 0.05).The serum H2S level and NSE level in FS group were negatively correlated (r =-0.279,P =0.024) ; There were significant differences of serum NSE level between seizure frequency less than twice group and seizure frequency greater than or equal to twice group(t =-2.955,P =0.004).The seizure frequency was negatively correlated with serum H2S level (r =-0.269,P =0.03),and positively correlated with serum NSE level (r =0.322,P =0.009).The seizure durations (≥ 5 min) was negatively correlated with serum H2S level (r =-0.532,P =0.019).Conclusion The serum H2S level is expected to be an objective index for eva-luating the seizure brain injury in the early period of FS,and also potentially the important occurrence factors of brain injury.
ABSTRACT
<p><b>OBJECTIVE</b>To study long-term behavioral and ultrastructural alterations in a hypoxic-ischemic brain damage (HIBD) model of neonatal rats.</p><p><b>METHODS</b>Sixty seven-day-old Sprague-Dawley rats were randomly subjected to unilateral carotid artery ligation followed by hypoxic exposure (HIBD group) or sham operation (n=30 each). A battery of behavioral tests, including Morris water maze test and sensorimotor tests, were performed at a postnatal age of 5 weeks. Nissl staining was used for counting neurons. Transmission electron microscopy was used for observing synapse structures and measuring the thickness of the postsynaptic density area and the length of the postsynaptic active area. The correlations of histological changes with the results of behavioral tests were evaluated.</p><p><b>RESULTS</b>The HIBD group showed a significantly longer escape latency (P<0.05) and a lower frequency of original platform crossing (P<0.05) in the Morris water maze test compared with the sham operation group. The sensorimotor function test showed that the sensorimotor function in the HIBD group was worse than in the sham operation group. Nissl staining showed that the number of neurons in the HIBD group was significantly reduced (P<0.01) compared with the sham operation group. Transmission electron microscopy showed that synapses were significantly reduced in number, and that the thickness of the postsynaptic density area and the length of the postsynaptic active area were reduced in the HIBD group. The thickness of the postsynaptic density area was negatively correlated with escape latency in the Morris water maze test (r=-0.861, P<0.01), and also negatively correlated with the total score of sensorimotor function tests (r=-0.758, P<0.05) in the HIBD group.</p><p><b>CONCLUSIONS</b>Hypoxia ischemia can lead to neuron loss and ultrastructure damage, resulting in long-term deficit of behavioral functions in neonatal rats.</p>