氯沙坦对维持性血透患者心血管保护作用的临床观察

目的 :观察氯沙坦对行维持性血透治疗的慢性肾功能衰竭 (CRF)患者心血管保护作用。方法 :6 0例维持性血透患者 (血肌酐≥ 70 0 μmol·L- 1 ) ,治疗组 (给予氯沙坦 5 0～ 10 0mg·d- 1 )及对照组 (给予非血管紧张素受体拮抗剂和非ACEI类降压药 )各 30例 ,记录用药前后各组患者血压 ,运用多普勒组织成像 (DTI)技术观察用药前后两组患者二尖瓣环峰值收缩速度 (VS)、收缩时间速度积分 (TVIS)、舒张早期速度 (VE)、舒张晚期速度 (VA)、VE VA 比值。结果 :治疗组及对照组患者治疗后血压均明显下降 ,二尖瓣环VS、TVIS、VE、VE VA ,则均明显上升 ;治疗组与对照组血压分别在治疗前、后相比并无明显差异 ;治疗前两组间二尖瓣环VS、TVIS、VE、VE VA 并无显著性差异 ,但在治疗12个月后 ,治疗组二尖瓣环VS、TVIS、VE、VE VA 则明显高于对照组。结论 :氯沙坦对行持续性血透的CRF患者具有良好的心脏保护作用 ,可有效改善其心功能 ,且不依赖于其降压作用     

球囊成形术后氯沙坦对兔血管内膜增殖及巨噬细胞表达的影响

目的　通过观察AT1受体的特异性拮抗剂氯沙坦 (Losartan)对兔腹主动脉球囊成形术后内膜增殖和巨噬细胞表达的影响 ,探讨氯沙坦治疗血管再狭窄的机制。方法　采用内皮剥脱加高脂饮食 (含 1 5 %胆固醇 )喂养 8周制作兔腹主动脉粥样硬化膜型 ,然后对狭窄部位行球囊成形术。术后氯沙坦组给予氯沙坦 10mg·kg-1·day-1口服 ,对照组喂生理盐水。 4周后取腹主动脉行组织形态学观察 ,用免疫组织化学方法分析巨噬细胞。结果　对照组内膜厚度 /中膜厚度比值为 0 65± 0 17,氯沙坦组则减少为0 44± 0 11(P <0 0 1) ,对照组内膜面积 /中膜面积比值为 0 74± 0 16,氯沙坦组则减少为 0 5 4± 0 13(P <0 0 1)。氯沙坦组新生内膜中巨噬细胞数亦较对照组显著减少 (P <0 0 1)。结论　氯沙坦通过抑制AngⅡ的作用进而抑制巨噬细胞的浸润 ,抑制炎症反应 ,从而减轻再狭窄     

缬沙坦对糖尿病大鼠心肌MCP-1表达的影响

目的　研究缬沙坦对糖尿病大鼠心肌MCP -1表达的影响。方法　将Wistar大鼠随机分成三组 :正常对照组 (NC组 )、糖尿病模型组 (DM组 )、糖尿病模型 +缬沙坦治疗组 (DV组 ) ,用STZ诱导糖尿病大鼠模型 ,于 8周后用免疫组织化学的方法检测糖尿病大鼠和缬沙坦干预的糖尿病大鼠心肌组织中MCP -1的表达。结果　 8周时心肌组织中MCP -1的表达DM组明显高于DV组、NC组 (P <0 0 1) ,DV组明显高于NC组 (P <0 0 1)。结论　缬沙坦能显著减少糖尿病大鼠心肌组织中MCP -1的表达     

吡那地尔对体外培养大鼠大脑皮层神经细胞缺氧缺糖损伤的保护作用

目的 :探讨ATP敏感性K+ 通道 (KATP)开放剂吡那地尔 (pinacidil,Pin)对缺氧缺糖再复氧损伤大鼠大脑皮层神经细胞的保护作用。方法 :体外培养大鼠大脑皮层神经细胞 ,细胞培养至 10d ,建立神经细胞缺氧缺糖损伤模型 ,观察Pin及KATP阻断剂格列苯脲对缺氧缺糖不同时间 ,再复氧 2 4h后细胞死亡率、丙二醛 (MDA)含量、超氧化物歧化酶 (SOD)活力的影响。结果 :缺氧缺糖、再复氧后大鼠的神经细胞死亡率均显著升高、MDA生成增多、SOD的活力下降 ,Pin干预后 ,细胞死亡率下降、MDA生成减少、SOD的活力升高 ;格列苯脲能拮抗Pin这种保护作用。结论 :Pin对缺氧缺糖损伤神经细胞具有保护作用 ,并与拮抗氧自由基有关     

Influence of mild hypothermia on vascular endothelial growth factor and infarct volume in brain tissues after cerebral ischemia in rats

BACKGROUND: It has been demonstrated that mild hypothermia has obvious protective effect on both whole and local cerebral ischemia. However, the definite mechanism is still unclear for the brain protection of mild hypothermia on cerebral edema, inhibiting inflammatory reaction, stabilizing blood brain barrier, etc. OBJECTIVE: To investigate the effect of mild hypothermia on the expression of vascular endothelial growth factor and the infarct volume after cerebral ischemia in rats, and analyze the brain protective mechanism of mild hypothermia. DESIGN: A randomized grouping and controlled animal trial. SETTING: Department of Neurology, People's Hospital of Yunyang Medical College. MATERIALS: Twenty adult male SD rats of clean degree, weighing (250±30) g, were provided by the animal experimental center, School of Medicine, Wuhan University. The kits for SP immunohistochemistry were purchased from Beijing Zhongshan Golden Bridge Biotechnology Co., Ltd. METHODS: The experiments were carried out in the laboratory of Department of Neurology, Renmen Hospital of Wuhan University from May to July 2005. ① The 20 rats were divided randomly into normal temperature group (n =10) and mild hypothermia group (n =10). Models of permanent middle cerebral artery occlusion were established with modified nylon suture embolization. The rats were assessed with the Longa standards: 0 point for without nerve dysfunction; 1 for mild neurological deficit (fore claws could no extend completely); 2 for moderate neurological deficit (circling towards the affected side); 3 for severe neurological deficit (tilting towards the affected side); 4 for coma and unconscious; 1-3 points represented that models were successfully established. The rats of the normal temperature group were fed at room temperature, and those in the mild hypothermia group were induced by hypothermia from 2 hours postoperatively, and the rectal temperature was kept at 34-35 ℃ for 72 hours. ② Measurement of infarct volume: All the rats were anesthetized by intraperitoneal injection overdose sodium pentobarbital 7 days postoperatively, and then the heads were cut down to harvest brain. The brain tissues were placed into -20 ℃ refrigerator for 20 minutes, coronal sections of 2 mm were prepared. The infarct sites were not stained, whereas normal brain tissues were stained as red. The infarct volumes were calculated by using MPLAS-500 multimedia color pathological image&&word analytical system. ③ Counting positive cells of vascular endothelial growth factor protein: The brains were harvested by cutting heads, then coronal sections of 2 mm were prepared. Routine dehydration, hyalinization, wax immersion and embedding were performed, then the detected with SP immunohistochemistry, the kits were purchased from Beijing Zhongshan Golden Bridge Biotechnology Co., Ltd. The cells whose cytoplasm was yellow-brown were positive ones, a single sample as a unit, peri-ischemic site and ischemic core were selected, and the corresponding sites in controlateral hemisphere were taken as controls. Five visual fields were selected from each site to be observed under microscope, the cells were counted, and the average number of positive cells was calculated in each group. The numbers of positive cells were determined with the image analytical apparatus. MAIN OUTCOME MEASURES: Number of the positive cells of vascular endothelial growth factor protein; Infarct volume of rat brain tissue. RESULTS: All the 20 rats were involved in the analysis of results. ① Number of positive cells of vascular endothelial growth factor protein in brain tissue: It was obviously lower in the mild hypothermia group than in the normal temperature group [(24.02±5.05), (36.07±2.69) cells/high power visual field, P < 0.01]. ② Comparison of infarct volume of brain tissue: After MCAO, it was obviously smaller in the mild hypothermia group than in the normal temperature group [(153.25±23.14), (253.45±36.21) mm3, P < 0.01]. CONCLUSION: Mild hypothermia can inhibit the expression of vascular endothelial growth factor and decrease the volume of cerebral infarction. The inhibition of mild hypothermia on the expression of vascular endothelial growth factor may be one of the brain protective mechanisms.     

参附注射液对肠缺血-再灌注大鼠肿瘤坏死因子α的影响

目的观察肿瘤坏死因子α(TNF-α)在大鼠肠缺血-再灌注损伤过程中的作用及参附注射液对TNF-α的影响,探讨参附注射液防治肠缺血-再灌注损伤机制。方法 SD大鼠随机分为肠缺血-再灌注组(IR组)、参附注射液预处理组(SF组)和假手术组(C组)。采用阻断肠系膜上动脉(SMA)的方法制造肠缺血-再灌注模型。分别测定各组动物血浆、肠组织TNF-α含量及血液动力学变化;光镜观察肠粘膜损伤情况。结果IR组再灌注后MAP下降,与C组和SF组比有显著性差异(P<0.01);SF组肠粘膜损伤程度减轻,与IR组比有显著性差异(P<0.01);SF组血浆及肠组织TNF-α水平降低,与IR组比有显著性差异(P<0.01)。结论参附注射液可明显防治大鼠肠缺血-再灌注导致的肠粘膜损伤,这种作用可能是通过抑制TNF-α的释放实现的。     

二尖瓣环钙化与颈动脉粥样硬化关系的超声研究

目的 了解二尖瓣环钙化（MAC）与颈动脉粥样硬化之间的关系，探讨MAC能否作为颈动脉粥样硬化的独立预测因子。方法 采用高频超声对156例MAC患者（其中55例为重度MAC患者）及118例年龄、性别与之相匹配的无MAC对照者的颈动脉进行了检测。结果 ①与对照组比较，MAC组及重度MAC组患者高血压和糖尿病的患病率明显增加（P〈0．05）；②MAC组颈动脉粥样硬化斑块发生率，颈动脉狭窄≥20％、≥40％及双侧颈动脉狭窄≥40％的发生率均显著高于对照组（P〈0．01），重度MAC组上述指标的改变更为显著（P〈0．01）。此外，重度MAC组颈动脉狭窄≥60％的发生率明显高于对照组（P〈0．05）；③MAC组及重度MAc组颈动脉内-中膜厚度（IMT）显著高于对照组（P〈0．01）；④单因素及多因素Logistic回归分析结果均表明：MAC是颈动脉狭窄≥40％最有意义的预测因子（P〈0．01）。结论 MAC与颈动脉粥样硬化之间存在十分密切的关系，通过对MAC的检测，能够预测颈动脉粥样硬化的存在及其程度，在临床实际工作中，对于有二尖瓣环钙化的患者应常规进行颈动脉粥样硬化的检查。     

白细胞介素6、信号传导和转录活化因子3和血管内皮生长因子在人脑胶质瘤中的表达及相关性研究

目的研究人脑不同级别胶质瘤中白细胞介素（IL）-6，信号传导和转录活化因子3（STAT3）和血管内皮生长因子（VEGF）的表达，探讨IL-6、STAT3和VEGF与肿瘤病理级别和侵袭性的关系。方法采用免疫组织化学法，检测70例人脑胶质瘤，10例脑膜瘤和5例正常脑组织中IL-6、STAT3和VEGF的表达。结果胶质瘤中IL-6、STAT3和VEGF的表达水平在高级别组（Ⅲ、Ⅳ级）明显高于低级别组（Ⅰ、Ⅱ级），两组间差异有统计学意义（P〈0．01），STAT3的表达与IL-6和VEGF的表达均呈正相关（P〈0．01）。结论IL-6、STAT3和VEGF的表达与胶质瘤的恶性程度有密切关系；且三者协同在胶质瘤发生、发展过程中起重要作用。三者的相关性证实VEGF基因由STAT3蛋白调节，而STAT3又由IL-6刺激活化。     

慢性乙型肝炎患者抗病毒治疗后生存质量评估

目的了解慢性乙型肝炎（CHB）患者生存质量（QOL）状况,并通过抗病毒治疗对其QOL进行干预.方法采用横断面调查,选择2003年至2004年期间武汉大学人民医院感染科212例慢性乙型肝炎患者及健康人群185例,分别以健康状况问卷（SF-36）、医学应对问卷以及肝病特质问卷进行调查.结果与健康对照组比较,CHB患者除情感职能（RE）外,其他维度得分均明显低于健康对照者（P＜0.05）.CHB患者QOL与年龄、肝病特质问卷得分以及医学应对问卷中的屈服、面对因子分显著负相关（P＜0.01）.虽然不同抗病毒治疗方案对CHB患者QOL的影响差异无统计学意义,但完全应答组与无应答组比较,两组除社会功能（SF）（P＜0.05）以外其他维度的得分差异均有统计学意义（P＜0.01）;部分应答组与无应答组比较,仅RE、躯体疼痛（BP）及一般健康状况（GH）维度的得分差异有统计学意义（P＜0.05）.结论CHB患者QOL多个纬度均有受损.有效的抗病毒治疗能提高患者的QOL.     

肠缺血/再灌注致肺损伤时肺内HO-1/CO与iNOS/NO相互作用的研究

目的观察肠缺血/再灌注(I/R)致肺损伤时肺内HO-1/CO与iNOS/NO的相互作用。方法采用肠缺血/再灌注模型。32只Wistar大鼠随机分为假手术组(Sham组)、肠缺血1 h再灌注6 h组(I/R组)、氨基胍组(AG组)和血晶素组(hemin组)。检测肺组织中HO-1和iNOS的表达,观察肺组织丙二醛(MDA)、血清一氧化氮(NO)及动脉血中氧血红蛋白(Hb-CO)的含量,同时观察肺组织病理形态学改变。结果与Sham组比较,I/R组HO-1和iNOS表达显著增强(均P<0.01);AG组HO-1和iNOS表达较I/R组明显降低(均P<0.05);Hemin组iNOS表达较I/R组明显降低而HO-1表达明显升高(均P<0.05);I/R组肺组织MDA、血清NO、血中HbCO较Sham组显著增加(P<0.05或P<0.01);与I/R组比较,AG组、Hemin组肺组织MDA、血清NO显著降低(P<0.05或P<0.01)。AG组的HbCO明显降低而Hemin组的HbCO明显升高(P<0.05)。病理学检查显示,AG组与Hemin组肺组织损伤程度较I/R组明显减轻。结论NO及CO对肠I/R肺组织具有保护作用,两者之间存在着相互作用,肺内HO-1/CO的大量生成具有使NO产生减少的作用,同时iNOS/NO的过量生成具有上调HO-1表达使CO产生增多的作用。