急性一氧化碳中毒迟发性脑病大鼠海马区长时程脑电信号研究

Long-Term Electroencephalogram Signal in Hippocampus of Rats with Delayed Encephalopathy Acute Carbon Monoxide Poisoning

急性一氧化碳中毒迟发性脑病(DEACMP)常见海马区病变,但假愈期该区域的病变过程和机制尚不清楚。因此,监测海马区长时程局部场电位活动,以探究DEACMP假愈期该区域脑电信号动态变化情况。选择30只雄性SD大鼠腹腔注射制备急性一氧化碳中毒大鼠模型,以周为节点于造模后1~8周分批在大鼠右侧海马区植入电极,每周采集4~5只大鼠海马区局部场电位信号,6只正常大鼠海马区局部场电位信号作为造模前参考基准,用小波包分解提取出α/β/θ/δ波,计算信号的均方根值(RMS)和能量占比。结果表明,与造模前相比,造模后前期(1/2周)和后期(7/8周)α/β/θ/δ波幅均显著增加(P<0.05),造模后1~8周期间4种振荡成分均方根值均呈现先增加后降低再增加的变化趋势。其中,造模前δ波波幅为(228±103)μV,造模后1和2周分别增加到(4751±4079)μV和(1616±1708)μV,7和8周则增至(1221±567)μV和(3222±2052)μV。模型组1~8周的δ波能量占比比造模前均显著增加(P<0.05),其中造模前δ波能量占比为0.50±0.09,造模后1~8周分别为0.62±0.14、0.65±0.12、0.77±0.13、0.73±0.12、0.59±0.11、0.70±0.11、0.71±0.11和0.89±0.08;且中后期5~8周δ波(α波)随病程进展逐步增加(下降)(P<0.05),α波造模前能量占比为0.10±0.04,造模后5~8周分别降至0.08±0.02、0.06±0.03、0.05±0.02和0.01±0.01。大鼠海马区4种脑电振荡均方根值在一氧化碳中毒初期普遍增加,预示DEACMP发病风险;中毒后δ波能量占比全程显著增加,且δ波和α波能量占比在中毒的中后期呈单向变化趋势。研究提示,脑电振荡分析方法可为DEACMP定量预测和评估提供一种新方法。

Delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)is a common pathological change in hippocampus,but the pathological process and mechanism in this area during the false recovery period are still unclear.Therefore,this study monitored the long-term local field potential activity in hippocampus to explore the dynamic changes of electroencephalogram signals in this area during DEACMP false recovery.Thirty male SD rats were injected intraperitoneally to make ACMP rat model,electrodes were implanted into the right hippocampus of rats in batches 1~8 weeks after modeling,and local field potential signals of hippocampus of 4~5 rats were collected every week.Local field potential signals of hippocampus of 6 normal rats were used as reference standard before modeling,and the RMS value and energy ratio ofα/β/θ/δwave were extracted by wavelet packet decomposition.Compared with that of before modeling,the amplitude ofα/β/θ/δincreased significantly in the early(1/2 week)and late(7/8 week)after modeling(P<0.05),and the root mean square values of four oscillation components showed a changing tendency of increasing first,then decreasing and then increasing from 1 to 8 weeks after modeling.Among them,theδwave amplitude before modeling was(228±103)μV,and in the 1 and 2 weeks after modeling,it increased to(4751±4079)μV and(1616±1708)μV.At the 7 and 8 weeks after modeling,the value increased to(1221±567)μV and(3222±2052)μV.The ratio ofδwave energy in the model group from 1 to 8 weeks increased significantly(P<0.05),among them,theδwave energy proportion before modeling was 0.50±0.09,and increased to0.62±0.14,0.65±0.12,0.77±0.13,0.73±0.12,0.59±0.11,0.70±0.11,0.71±0.11 and 0.89±0.08 after modeling 1~8 weeks,respectively.In the middle and late stage(5~8 weeks),theδwave(αwave)gradually increased(decreased)with the progression of the disease(P<0.05).Before modeling theαwave energy ratio was 0.10±0.04,and after modeling(5~8 weeks)it decreased to 0.08±0.02,0.06±0.03,0.05±0.02 and 0.01±0.01,respectively.The RMS values of the four kinds of electroencephalogram oscillations in the hippocampus of rats generally increased the risk of DEACMP in the early stage of carbon monoxide poisoning.After poisoning,the energy proportion ofδwave increased significantly throughout the poisoning,and the energy proportion ofδwave andαwave changed unidirectional in the middle and later stages of poisoning.The study provided a new method for the quantitative prediction and evaluation of DEACMP.