| Objective The methods used for preventing sudden cardiac death have been documented not to do well. A lot of drugs for severe arrhythmia may promote severe arrhythmia and increase mortality rates instead of what expected. Looking for the effective methods for improving prognosis of myocardial infarction (MI) has become the research subject that is urgent to be resolved in the fields of the cardivascular researches. The past several years have witnessed the recognition that fastigial nucleus stimulation (FNS) has neuroprotective effects against damage of ischemia and the others, including supressing neuronal apoptosis and promoting nerve tissue construction. One-hour electrical stimulation of fastigial nucleus (FN) can decrease infarction volume by 50% on average in cerebral infarction. It was reported that electrical stimulation of FN percutaneously in rats with local cerebral infarction had the similar effect as stimulation of FN directly, which was demonstrated by the electrical signal coming from the concentric circular electrode. The demonstration of similar effect of the direct or indirect FN stimulation implies that in vitro administration of percutaneous FNS could be of clinical relevance. Recently , cerebellum electric stimulation devices , which start from experimental FNS and minic biological electric current have used in clinical practise for treating a lot of diseases. It was confirmed that FNS significantly improved heart rate variability (HRV) or increased vagal activity on patients with cerebral infarction.Now it has been confirmed that reduced HRV as quantitative markers of autonomic nervous state is closely related to the overall postinfarction mortality and sudden cardiac death. Previous studies of FNS spurred efforts to explore the effect of FNS on HRV and cardiac nerve regeneration after MI in this study. Further, we investigate the effects of FNS on NGF,inflamatory cytokines genes expression and production of oxygen free radical as well as levels of nerve transmitters in post-MI hearts.Methods Animal models were created by stimulating FN with the flow of electricity, using ibotenic acid to produce lesions of FN neurons, ligating the left anterior artery (LAD), respectively. Wistar rats were randomly divided into four groups: group MI was rats with myocardial infarction alone; group FNS+MI was rats receiving FN stimulation for 1 hour before producing MI; group FNL+FNS+MI was rats undergoing the same procedure like group FNS+MI except that there were lesions of the FN five days before producing MI; group Sham was rats without ligating LAD and stimulating FN, just mimicing all the operations. Then every group was randomly divided into three subgroups according to the three time points, that is 1,7,21 days after MI for further study. Power spectral density (PSD) was measured by the HRV recording and analysing equipment; survial rate was calculated; sympathetic or vagal nerve fibers density in the infarcted zone(IZ) and non-infarcted zone(NIZ) were examined by immunohistochemistry ; the mRNA expression levels of NGF, TNF-α,IL-1β and IL-6 in IZ and NIZ were studied by RT-PCR; the infarction area was measured by nitroblue tetrazalium(NBT) staining method; cardiac norepinephrine(NE) content was measured with high performance liquid chromatography(HPLC); the activities of acetylcholinesterase (ACHE),superoxide dismutese (SOD) ,content of malondialdehyde (MDA) and total anti-oxidative capability (TAOC) in cardiac tissues as well as serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities were measured with biochemistry method.Results The main results were as follows:1. Effect of FNS on the HRV in ratsLF, HF, HFnorm and FD at day 1, 7, 21 after MI were significantly reduced compared with the Sham group; LFnorm and LF/HF increased significantly. Electrical stimulation of the FN could increase LF, HF, HFnorm, FD and decrease LFnorm, LF/HF at each time point. There showed no obvious effect on the HRV after lesion of FN in advance. 2. Influence of...
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