Experiment Study Of Protective Effect Of Transcranial Magnetic Stimulation On Focal Cerebral Ischemic Rats

PART ONEObject: To study the effect of transcranial magnetic stimulation (TMS) on the expression of basic fibroblast growth factor(bFGF) and Tie-2 in middle cerebral artery occlusion/reperfusion(MCAO/R) rats, and explore the mechanism of TMS on neovascularization after MCAO/R.Methods: TMS group and sham group each with 30 rats accepted 1 session of TMS(200pulse) and sham TMS respectively within 3 weeks after MCAO/R. The expression of bFGF and Tie-2 by immunohistochemical staining was observed. Carry on statistical analysis to the acquire data.Results: 3 weeks later, the neurological deficit scores of TMS group were reduced obviously compared with sham TMS group (P<0.01) .After MCAO/R 1 day, the count of bFGF immunity positive cells in cortex around the infarction focus of TMS group were more than those of sham TMS group, but there were no remarkable difference(P>0.05). While MCAO/R 3 days,7days,14days and 21 days, the expression of bFGF immunity positive cells in the TMS group were significantly higher compared with sham TMS group(P<0.01).And there was significant reverse correlation between the count of bFGF immunity positive cells and neurological score of two groups(r=-0.791,P<0.01). At each time point, the expression of Tie-2 immunity positive cells in TMS group were slightly higher than those in sham TMS group,and the increase of Tie-2 was not significant(P>0.05).Conclusion: TMS can promote the restoration of neurological deficit and angiogenesis in MCAO/R rats. The mechanism is partly correlated with the expression of bFGF immunity positive cells, but there no significant correlation with the expression of Tie-2 immunity positive cells. PART TWOObjective: To study the mechanism of TMS on reducing cerebral edema in MCAO/R rats by measuring apparent diffusion coefficient in the infarct core and infarct margin.Methods: TMS group and sham TMS group each with 6 rats accepted 1 session of TMS (200 pluses) and sham TMS per day respectively within 7 days after MCAO/R. MR imaging was performed at 1hour, 3 hours, 24 hours, 3 days and 7days after MCAO/R. The sequences included T1WI, T2WI and DWI., and the apparent diffusion coefficient(ADC) graph was re-established by computer. Parameters measured included ADC of infarct core and infarct margin, and ADC of collateral normal brain. The relative ADC was calculated. To measure the high signal areas per slice at each examination point, then the lesion volume of cerebral ischemia was acquired by calculating. Statistical analysis was performed by SPSS 13.0 software package.Results: At each examination tine, rADC in infarct core was lower than normal. Within 3 days after MCAO/R, rADC in infarct margin was lower than normal, and 7 days later, rADC equaled approximatively with normal.,and even was higher than normal. Whatever in infarct core or margin, rADC of TMS group was higher than rADC of sham TMS group at each time point. In each group, rADC of infarct core was always higher than it of infarct margin. At 1 hour after MCAO/R, rADC in infarct core and margin of TMS group had no significant difference compared with sham TMS group(P>0.05). At 3 hour after MCAO/R, in infarct core and margin, rADC of TMS group was significantly higher than it of sham TMS group(P<0.01). At 24 hour, in infarct core, rADC of TMS group raised magnificently higher than it of sham TMS group(P<0.01); in infarct margin, rADC of TMS group was higher than it of sham TMS group(P<0.05). While 3 days and 7 days later, there no significant diffenence between two groups(P>0.05). The lesion volume of cerebral ischemia showed significant diffenence between two groups at 24 hour and 7 days after MCAO/R.Conclusion: TMS can effect the diffusion of hydrone in cortex around the infarction focus, then extenuate cerebral edema.