| Vascular dementia (VD) refers to an acquired, generalized, and often progressive impairment of cognitive function caused by cerebrovascular lesion. VD is one of the most common cause of dementia in Old-age,which is severely harmful to the physical and mental health, as well as a heavy load to the society. Because VD is somewhat reversible, it is valuable to study the pathogenesis.Up to now there are many theories about the pathogenesis of VD, but no one can explain the process precisely. The relationship between cerebral infarction and dementia has been extensively investigated. With the profound consideration about pathogenesis of VD,the abnormal cerebral blood flow(CBF) and metabolism proved to be especially important in the process and widespread white matter lesion could lead to VD. The pathophysiological mechanism responsible for Subcortical white matter lesions is generally believed to be chronic cerebral hypoperfusion. However, The effects of ischemia on the cerebral white matter structure seldom have been studied. This study illustrated some of the pathophysiological processes of VD from the aspects of behavior, rCBF and pathology on cortex and subcortical white matter.150 Male Wistar rats weighing 300 to 350 g were used in this experiment and randomly divided into experimental and control subjects. 1)We established a VD rat model after chronic Cerebral Hypoperfusion caused by permanent bilateral common carotid arteries(CCA) occlusion. 2) PeriFlux5000　laser doppler flowmeter(LDF)was used to detect the CBF of frontal cortex,parietal cortex,Hippocampus and subcortical white matter at predetermined time intervals(1,2,3 and 4 months after the occlusion of the CCA). 3) Morris water maze experiment was adopted to test the rats memory change of each group. The escape incubation period express the rats memory ability. 4) Brain samples with HE and LFB staining from frontal lobe,temporal lobe,Hippocampus and the white matter were examined with light microscopic methods at 1, 2, 3 and 4 months after the operation. 5) The abnormalities of white matter nerve fibre bundle were quantified with an image-analysis system. 6) The data were analyzed by means of t test and multiple factor analysis of variance.In this time-dependent study of the VD animal model induced by CCA occlusion of up to 4-month duration, we document widespread injury to both cortex and the white matter. 1) The rCBF-lesion caused by CCA occlusion could be observed. At 1 month the CBF of frontal cortex,parietal cortex and Hippocampus reduced obviously. As late as 4 months after CCA occlusion, the CBF of frontal cortex,parietal cortex,Hippocampus and Subcortical white matter descended to 25.78%,79.02%,66.4%,53.76%. 2) The rats with CCA occlusion performance showed their memory ability decreased from one month after operation. Until 4 months no recovery of the operated rats intelligence has been seen. The Comparison between 4 experimental groups showed no statistical difference. 3)There were obvious histopathological changes in the brain after the chronic cerebral hypoperfusion. With the CBF decrease, the pyramidal cell of frontal cortex,temporal lobe and Hippocampus appeared ischemic changes, such as pyknosis, denaturation, necrosis and degeneration; small vessels proliferation; the proliferation of gliacytes generally existed to form glial nodes; damages of the nerve fibers and myelin sheath were found in the white matter under the cortical layer. The changes mentioned above became more sever along with the elapse of time.Permanent bilateral CCA occlusion can exactly cause experimental rats persistent chronic cerebral hypoperfusion; irreversible cognitive impairment could been seen accompanied with the decrease of CBF; persistent chronic cerebral hypoperfusion resulted in widespread histopathological changes. That suggests the chronic, progressive CBF decrease is the major cause of the VD occurrence. The degenerative changes resulting from chronic hypoperfusion of the brain are the pathological basis of the l... |
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