Objective To observe the patients with subcortical cerebral infarction in the acute period, disabled in the motor function, and explore the extent of impact of several predictive factors to the recovery of motor function, including diffusion tensor imaging (DTF) displaying the involving extent of pyramidal tract, in order to find the most reliable and closely predictors. Methods 82 patients with acute cerebral infarction and disability (mRS score ≥ 3 points) were followed up on the 90 d after the symptom onset, respectively. Combining the baseline clinical characteristics, the laboratory and imaging auxiliary examination and treatment methods, choosing gender, age, hypertension, diabetes, hypercholesterolemia,atrial fibrillation or angina history, smoking history, alcohol history, the initial disability level,homocysteine, C-reactive protein, treatment modalities, the volume of infarction and the involving extent of pyramidal tract as observed indicators. According to mRS result, the outcome of the patients were divided into disabled groups ( mRS 3-5) and non-disabled group ( mRS 0-2). Results Using chi-square test to make univariate analysis, results showed that age (χ2 = 47.492, P ＜ 0. 01 ), diabetes ( χ2 = 5. 126, P =0. 024), hypercholesterolemia(χ2 =6. 242 ,P = 0. 012), the initial degree of disability (χ2 =45. 359, P ＜0. 01 ) and the involving extent of pyramidal tract (χ2 = 51. 467, P ＜ 0. 01 ) could effect patients gaining recovering. Using multivariate Logistic regression analysis to make a multivariate regression analysis, results suggest that age ( OR = 0. 068, P = 0. 042), the involving extent of pyramidal tract ( OR = 0. 026, P = 0. 002 )are independent predictors of recovery of motor function in patients, diabetes mellitus, hypercholesterolemia,initial disability level have no significant correlation. Conclusion The involving extent of pyramidal tract reflected by DTT is the best predictor of recovery in patients with subcortical cerebral infarction in the acute period.

Aim To investigate the effects of an angiotensin Ⅱ receptor blocker,candesartan, on aorta oxidative stress-LOX-1 pathway in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP).Methods 12-week-old salt-loaded SHRSP were treated with candesartan(1.0 mg?kg-1?d-1)or a diuretic, trichlormethiazide(TCM,1.6 mg?kg-1?d-1) or no treatment(n=6) in each for 2 weeks. Age-matched salt-loaded WKY rats were served as control(n=6).Systolic blood pressure(SBP)was measured weekly throughout the 2-week period by means of the tail-cuff method.Thoracic aortas were extracted and 24 h urine was collected.NAD(P)H oxidase subunits(p22 phox, p47 phox and gp91 phox)mRNA expression in aorta were assayed by real-time PCR. LOX-1 and type Ⅳ collogen mRNA expression were examined by RT-PCR. gp91 phox and LOX-1 protein expression in aorta were assayed by immunohistochemistry.Urinary albumin excretion was examined by ELISA.Results At the end of the 2nd week, SBP was significantly higher in salt-loaded SHRSP than that in salt-loaded WKY rats. Treatment with candesartan and TCM significantly decreased SBP in salt-loaded SHRSP at similar levels.NAD(P)H oxidase subunits (p47 phox and gp91 phox)and LOX-1 mRNA expression in aorta were markedly higher in salt-loaded SHRSP than those in salt-loaded WKY rats.Candesartan and TCM had the effect of reducing the systolic blood pressure at similar levels. Candesartan significantly down-regulated aorta p22 phox, gp91 phox,LOX-1 and type Ⅳ collogen mRNA expression and decreased urine albumin excretion in salt-loaded SHRSP(P

AIM: To investigate the effect of fluvastatin on the proliferation of vascular smooth muscle cells derived from spontaneously hypertensive rats. METHODS: The aorta smooth muscle cells(ASMCs) of spontaneously hypertensive rats were cultured, and proliferation of cells were detected by measuring cell number and -thymidine(-TdR) incorporation after incubation with Ang Ⅱ, PDGF, fluvastatin and mevalonate acid. RESULTS: (1) The increased cell number and -TdR incorporation stimulated with AngII(10 -6 mol/L) and PDGF(10 ?g/L) were significantly inhibited by fluvastatin in a concentration-dependent manner (10 -5 -10 -7 mol/L); (2) The inhibitory effect of fluvastatin was almost completely reversed by mevalonate acid(10 -3 mol/L). CONCLUSION: The proliferation of ASMCs induced by Ang Ⅱ and PDGF was inhibited by fluvastatin, suggesting that mevalonate acid pathway may play an important role in the proliferation of ASMCs.