论文部分内容阅读
目的观察电刺激小脑顶核(FNS)对脑源性自主神经活性的保护作用。方法以大鼠右侧大脑中动脉阻塞为模型,用心率变异性(HRV)分析方法,观察脑梗死大鼠的心率变异性变化;将脑梗死大鼠随机分成非小脑顶核毁损组和梗死组,观察两组大鼠的心率变异性的频域和混沌参数值;用兴奋毒性物质鹅膏氨酸预先毁损两侧小脑顶核后,观察FNS对脑梗死大鼠的心率变异性的影响。结果大鼠脑梗死后,心率变异的频域和混沌参数值降低,与假手术组比较差异有统计学意义(P<0.05);当电刺激非小脑顶核毁损组大鼠小脑顶核时,发现心率变异的频域参数值、混沌参数值逐渐增加,与脑梗死组比较差异有统计学意义(P<0.05);预先毁损小脑顶核后,电刺激脑梗死大鼠小脑顶核,心率变异的参数值无明显变化,与非小脑顶核毁损组比较差异有统计学意义(P<0.05)。结论FNS可提高大鼠脑梗死后自主神经活性。这可能是其对抗缺血性脑损伤改善自主神经活性的脑保护作用之一。
Objective To observe the protective effect of electrical stimulation of cerebellar fastigial nucleus (FNS) on brain-derived autonomic nerve activity. Methods The model of right middle cerebral artery occlusion (MCAO) in rats was used as the model. Heart rate variability (HRV) was used to observe the changes of heart rate variability in the rats with cerebral infarction. The rats were randomly divided into non-cerebellar fastigial nucleus lesion group and infarct group The frequency-domain and chaos parameters of heart rate variability of the two groups were observed. The effect of FNS on the heart rate variability of cerebral infarction rats was observed by pre-lesioning the cerebellar fastigial nucleus with the excitotoxic substance goose. Results After the cerebral infarction in rats, the frequency-domain and chaos parameters of heart rate variability decreased significantly compared with the sham operation group (P <0.05). When the cerebellar fastigial nucleus was electrically stimulated in the non-PCN rats, Found that the frequency domain parameters of heart rate variation, chaotic parameter values gradually increased, compared with the cerebral infarction group was statistically significant (P <0.05); pre-damaged cerebellar fastigial nucleus, electrical stimulation of cerebral infarction rat cerebellar fastigial nucleus, heart rate variability No significant changes in parameter values, compared with the non-cerebellar fastigial nucleus damage group was significantly different (P <0.05). Conclusion FNS can improve autonomic nervous activity after cerebral infarction in rats. This may be one of the brain protective effects against ischemic brain damage that ameliorates autonomic nervous activity.