| Background and Objective:Although cerebral ischemia especially multi-cerebral infarction has been proved to be the main cause of vascular dementia (VD), one of the main type of senile dementia, its pathogenesis needs further study. On the other hand, it's difficult to conform the relationship between vascular diseases and dementia and to treat the cognitive handicap from VD just as those from AD.Recently, an abnormal TH level in serum, maily low T3 syndrome, was found in patients with VD from clinical investigation, and its changes correlate to level of dementia. But there are few treatment of TH to low T3 syndrome from nervous system diseases and no animal study among the documents. In this study, a rat model of chronic cerebral ischemia was esteblished through permanently Bilateral common carotid artery ligation. The rats' praxiology changes, TR and Ach content in brain tissue during different level of TH in vivo were determined in order to further disclose the relationship between TH system and cognitive dysfunction from chronic cerebral ischemia and to give new theory to the theropy of VD.Method:?0 Sprague-Dawley (SD) male rats were random divided into 5 groups: i.e. the normal group (control); the purely operation group (PO, permanently Bilateral common carotid artery ligation was performed for 5 weeks); the acute phase treatment group (APT, the rat was feed with TH (20mg per rat per day) from the next day of the operation for 5 weeks); the chronic phase treatment group (CPT, the rat was feed with TH (20mg per ratper day) 35 days after the operation for 5 weeks); and the hypothyroidismvgroup(HT, the rat was provided with iodine deficient feeds containing 0.15% thiopropyl for 8 weeks).Morris Water Maze Test: place orientation, special probe(twice in the CPT before and after treatment) and working memory test was performed t.and brain TR (include Kd, Bmax) was detected using Radioreceptor assay (RJRA) by the end of experimen. The other research items include TH in serum, acetylcholine (Ach) in brain, hematoxylin and eosin staining(HE) and Bielschowsky's improved argentation staining(Ag).(3)One-way ANOVA was used to estimate the item differences among the groups using SPSS 10.0 for Windows.Result:Pathologic study: 5 weeks after bilateral common carotid artery ligation, the neurons in cerebral cortex and CA3 area of hippocampus shrinking, decreasing, triangle nucleus and bow around nucleus cound be seen during HE Staining; the glia in those areas increased, part of the chromatins rarefied looking like "gitter cell". The pathologic changes worsened 8 weeks after the operation: more pyramidal cells in cerebral cortex and hippocampus decreased, and more "corynecells" could be seen. There were no abnormal changes seen in HT during HE and Ag staining and no obvious softening focus in the same areas.(D Praxiology study: The latent period was 6.19 ?.90s in normal control, 9.70 ?.87s in HT, 57.87 ?57.48s in PO, 16.13 +19.50s in APT and 25.16+27.12s in CPT during place orientation test(the latent periods of PT were longer than that of the other groups(p<0.05),and there were no significant difference among the rest groups ).The probe time was 32.18 +VI7.17s in normal control, 29.60?.13s in HT, 18.50?.05s in PO, 20.58?7.99s in APT and 19.38?.80s in CPT during spacial probe test(The probe time of normal control and HT was shorter than that of PO, APT and CPT during spatial probe test (p<0.05), and the score of PO was poorest among groups); and there were no significant difference between before (27.56+ 9.44s) and after (19.38?.81s)the treatment in CPT. The latent period was 5.78?.27s in normal control, 8.43?.52s in HT, 62.84?0.26s in PO, 12.65 +12.79s in APT and 33.57 + 23.38s in CPT during working memory test(The average latent period of PO and CPT was longer than that of the other groups (p<0.05), and the score of PO was poorest among groups once more.).(3)T3 were zero in all groups. T4 (nmol/L) were zero in HT, 54.85 + 21.13 in normal control, 29.42 + 7.84 in PO, 31.99 + 13.29 in A... |
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