Objective: To explore the formative mechanism of the syndrome of blood stasis in cerebra venation of senile vascular dementia and to investigate Danlong Xingnao Pill's(DLXNP) intervenient effects on it.Methods: The experimental aged SD (Sprague-Dauley) rats were divided randomly into 5 groups: normal group, sham operation group, cerebral ischemia reperfusion group, DLXNP group and nimodipine group. Besides the normal group and the sham operation group, each of the rats was repeatedly ischemia and reperfusion for two times combined after intraperitneal injection of sodium nitroprusside to establish the vascular dementia models. After giving sodium nitroprusside, bilateral carotid arteries (CCA) were occluded with artery clips for two times, every time for 10 minutes, brains were recirculated for 10 minutes by removal of clips between the two times. Water maze test and step-down avoidence test were used to messure learning and memory ability from the 8th day after the operations. Extracted materials from brains at the 12th day after the operations, and then made paraffin section and HE staining so as to make observation on hippocampal cell pathomorphology, hippocampal cells number was counted. The effects ofDLXNP on cerebral SOD, MDA, Ca +, excitatory amino acids(EAAs), blood rheologie characteristics were detected.Results:After cerebral ischemia reperfusion compared with thenormal group and the sham operation group, the cerebral ischemia reperfusion group's learning and memory ability decreased, the SOD activity decreased dramatically; whereas, the concentrations of Glu, Asp, Ca +, the contents of MDA increased, hippocampal cells number decreased. When detected 8 days after the operations, compared with the cerebral ischemia reperfusion group, DLXNP group's learning and memory ability increased. When detected 12 days after the operations, blood rheologie characteristics improved, the SOD activity increased; the contents of Glu, Asp, MDA, Ca2+ decreased and hippocampal cells number is more than those of cerebral ischemia reperfusion group. There is no dramatical difference between the effects of the nimodipine group and the DLXNP group.Conclusion: After the cerebral ischemia reperfusion, free radical metabolism became foul-up, excitatory neurotoxicity of EAAs improved, calcium overloaded, blood rheologie characteristics became worse. Perhaps it is the formative mechanism-athological serial reactions of the blood stagnant in cerebral venation syndrome of VD. Composed in the way of activating the blood and eliminating the stagnant, DLXNP has the function of protesting hippocampus region from cerebral ischemia reperfusion injury and improving learning and memory ability deficit through improving blood rheologie characteristics, regulating EAAs and relieving its excitatory neurotoxicity, improving oxygen free radical metabolism, reducing intracellular calcium overload. Which may be one of the mechanisms the actions of DLXNP.
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