Abstract
Objective To evaluate the role of Na+ -K+ -2Cl- cotransporter isoform 1(NKCC1)in neurons in sevoflurane-induced epileptiform electroencephalogram(EEG)activity in the cortex of neonatal rats. Methods Twenty-four neonatal Sprague-Dawley rats, aged 4-6 days, weighing 8-15 g, were randomly divided into 3 groups(n=8 each)using a random number table: control group(group C), sevoflurane group(group S), and NKCC1 inhibitor bumetanide + sevoflurane group(group B). After electrodes were placed correctly, EEG was monitored continuously.At 30 min of monitoring, normal saline 3 μl/g was injected intraperitoneally in D and S groups, and bumetanide 10 μg/g was injected intraperitoneally in group B. At 60 min after the end of intraperitoneal administration, anesthesia was induced with inhalation of 6% sevoflurane for 3 min and maintained with inhalation of 2.1% sevoflurane for 1 h in group S and group B. The total duration of seizures, the duration of a single episode, the number of episodes of electroencephalographic seizures, and the amplitude and frequency of spike-and-wave were recorded. Results Seizures were not detected in group C, and no spike-and-wave was found in group B. Compared with group C, the incidence of seizures in S and B groups(75% and 25%, respectively)and incidence of spike-and-wave in group S(100%)were significantly increased(P<0.05). Compared with group S, the incidence of seizures and spike-and-wave was significantly decreased, the total duration of seizures, and duration of a single episode were significantly shortened, and the number of episodes of electroencephalographic seizures was significantly decreased in group B(P<0.05). Conclusion NKCC1 in neurons may be involved in the formation of sevoflurane-induced epileptiform EEG activity in the cortex of neonatal rats. Key words: Anesthetics, inhalation; Infant, newborn; Electroencephalography
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