ABSTRACT
Objective To evaluate the correlation between serum uric acid with cognitive disorder after acute cere?bral infarction by prospective study. Methods Four hundred consecutively enrolled patients of acute cerebral infarction were divided into no cognitive impairment group and cognitive impairment group according to the assess of Montreal Cog?nitive Assessment (MoCA). Univariate analysises were conducted in the potential risk factors of cognitive impairment in?cluding age, sex, smoking, alcohol, hypertension, diabetes, dyslipidemia, level of education, infarction in key parts, atrial fibrillation, serum uric acid, blood homocysteine between two groups. The statistically significant indicators in univariate analysises were used as independent variables and the scores of MoCA were used as the dependent variable to conduct multiple linear regression analysis. The assessment on the risk of cognitive impairment after cerebral infarction were con?ducted according to serum uric acid, sex, age and TOAST classification further. Results Serum uric acid was indepen?dent risk factors of cognitive disorder after acute cerebral infarction. The risk of cognitive disorder after acute cerebral in?farction was significantly increased in patients with high level of serum uric acid than with normal level and the relative risk was 1.35,95%CI(1.098,1.660). Especially for the young, male or patients with cerebral infarction in classification of small artery occlusion, the risk increased further, and the relative risk was 1.513, 95%CI(1.092, 2.096)1.412, 95%CI (1.125, 1.771)and 1.464, 95%CI(1.128, 1.900)respectively. Conclusion Exaltation of Serum uric acid was indepen?dent risk factor of cognitive disorder after acute cerebral infarction. The risk of cognitive disorder after acute cerebral in?farction was significantly increased in patients with high level of serum uric acid than with normal level, and especially for the young, male and patients with cerebral infarction in classification of small artery occlusion, the risk increased fur?ther.
ABSTRACT
BACKGROUND: Endothelial cell structural and functional integrity is importnat decisive fatcor for ischemic time-window and hemorragic transformation follwing brain ischemic injury.OBJECTIVE: To investiagte the endotheliocyt endurance to various course of ischemic injury basing on dynamical observation of morphological and ultrastructural changes of endotheliocyte during IR injury.DESIGN: Randomized controlled experiment.SETTING:Neurological Internal Department of the Second Affiliated Hospital of Jinan University.MATERIALS: This experiment was carried out in the Animal Experimental Laboratory of the Second Affiliated Hospital of Jinan University from March 1998 to March 1999. Totally 53 SD rats were randomly dihours of 6 rats.METHODS: Thread-bolt occlusion method was used to establish focal brain ischemia model on rats. Brain tissue was evenly cut into five coronary segments: namely A, B, C, D and E, segments C underwent TTC staining for marginal region location. segments D was taken for routine dehydration, transparency, envelop, slice and HE staining,optical microscopic observation. Ischemic surrounding area and central brain tissues was obtained from slice B, fixed and enveloped before cutting into ultrathin slices that was observed under transmission electron microscope.the occurring time of hemorrhagic infarction at different ischemic time cell vacuolization degree in foot process layer at different ischemic time points.RESULTS: Totally 53 rats were enrolled in this experiment and all data was entered into results analysis. Under optical microscope: Neuropil loose and small vascular surrounding edema was observed at ischemia 3 hours.Small arterial broken and hemorrhage occurred at ischemia 12 hours reperfusion 3 hours. Under electron microscope: Capillary endothelial nuclear swelling was observed at ischemia 3 hours, with cytoplasmic pinocytosi increasing and vacuolization in foot process layer appearing+; At ischemia 3 hours reperfusion 3 hours, the foot process layer vacuolization in center area was (++) and (+++) in marginal area; while at ischemia 6 hours reperfusion 3 hours, endothelia tight junction opened and vacuolization in foot process layer was (+++); pinocytosis was found obviously reduced after ischemia 12 hours reperfusion 3 hours, mitochondrial swelling was seldom observed, but tight junction increasingly opened and vacuolization in foot process layer appeared (+++) - (++++).CONCLUSION: Obvious structural changes of endotheliocyte appeared in post-ischemia 3 hours, endotheliocyte tight junction openning was observed at ischemia 6 hours, and hemorrage transformation occurred after ischemia 12 hours, mainly at the post-reperfusional ischemia center.