尼莫地平联合卡维地洛治疗原发性高血压78例临床分析

目的分析尼莫地平联合卡维地洛治疗原发性高血压的临床疗效。方法将150例原发性高血压随机分成两组,对照组给予尼莫地平治疗,治疗组在对照组治疗的基础上,加之卡维地洛。结果治疗组与对照组显效率分别为33.3%和26.4%,总有效率为88.5%和76.4%,两组相比具有显著性差异（P〈0.05）。结论尼莫地平联合卡维地洛治疗原发性高血压疗效更为显著。     

高危患者降压治疗:重视控制血压底线

高血压高危患者的降压治疗既需降低血压，又需保持足够血流以保障器官灌注。血压降低过度无疑也有一定风险，因此控制皿压需要底线。高危高血压患者的个体差异大，在降压治疗过程中，临床医生既要以循证医学为鉴，叉须遵循个体化治疗原则，把握好降压幅度和速度，坚持高质量平稳降压，才能更好地保护靶器官，减少心脑血管意外的发生。     

暴发性急性胰腺炎并发腹腔室隔综合征临床诊治进一步探讨

目的探讨暴发性急性胰腺炎并发腹腔室隔综合征的治疗方案。方法回顾性分析1998年1月至2007年3月共收治FAP并发腹腔室隔综合征31例的诊治经验，对收治的31例暴发性急性胰腺炎并发腹腔室隔综合征患者根据腹腔内压力、腹腔室隔综合征分型，以及早期（发病后3d内）手术治疗与非手术治疗结果进行总结。结果31例暴发性急性胰腺炎并发腹腔室隔综合征患者13例行非手术治疗，其中轻度腹腔室隔综合征者5例（死亡1例），中、重度8例（死亡4例）；3d内早期手术治疗18例，其中轻度腹腔室隔综合征者5例（死亡2例），中、重度13例（死亡4例）。当腹腔内压力〉21mmHg时，早期手术治疗组死亡人数明显低于早期非手术治疗组（P〈0．05）。根据ACS分型，Ⅰ型非手术治疗5例（死亡2例），Ⅱ型非手术治疗4例（死亡2例），Ⅲ型非手术治疗4例（死亡2例）；Ⅰ型手术治疗9例（死亡2例），Ⅱ型4例（死亡2例），Ⅲ型5例（死亡2例）。Ⅰ型手术治疗组死亡人数明显低于非手术治疗组（P〈0．05），Ⅱ、Ⅲ型两组手术治疗组与非手术治疗组比较，死亡人数差异无统计学意义（P〉0．05）。结论当腹腔内压力〉21mmHg，且CT提示为Ⅰ型ACS的FAP患者，宜尽早行有效的腹腔减压引流；而对于腹腔内压力〉21mmHg，CT提示为Ⅱ、Ⅲ型ACS的FAP患者，早期手术减压效果有待进一步观察。     

Diabetes mellitus, hypertension and medial temporal lobe atrophy: the LADIS study.

HYPOTHESIS: Based on recent findings on the association between vascular risk factors and hippocampal atrophy, we hypothesized that hypertension and diabetes mellitus (DM) are associated with medial temporal lobe atrophy (MTA) in subjects without disability, independent of the severity of white matter hyperintensities. METHODS: In the Leukoaraiosis And DISability in the elderly (LADIS) study, we investigated the relationships between DM, hypertension, blood pressure and MTA in 582 subjects, stratified by white matter hyperintensity severity, using multinomial logistic regression. MTA was visually scored for the left and right medial temporal lobe (score 0-4), and meaned. RESULTS: Mean age was 73.5 years (sd 5.1), 54% was female. Of the subjects, 15% had DM, and 70% had a history of hypertension. The likelihood of having MTA score 3 was significantly higher in subjects with DM (OR 2.9; 95% CI: 1.1-7.8) compared with an MTA score of 0 (no atrophy). The odds ratio for MTA score 2 was not significantly increased (OR 1.8; CI: 0.9-4). Systolic and diastolic blood pressure and a history of hypertension were not associated with MTA. There was no interaction between DM and hypertension. Stratification on white matter hyperintensities (WMH) did not alter the associations. CONCLUSION: Our study strengthens the observation that MTA is associated with DM, independently of the amount of small vessel disease as reflected by WMH.     

两种艾灸法对二肾一夹型高血压大鼠血压和血管内皮细胞内分泌功能的影响

目的:应用两种艾灸疗法治疗两肾一夹肾血管性高血压大鼠(2K1C-RHR),评价这两种艾灸疗法的降压作用,并对其降压机理作初步的探讨。方法:建立2K1C-RHR模型,并将其随机分为六组:灸法Ⅰ组(百会、神阙、足三里)、灸法Ⅱ组(关元、涌泉、足三里)、卡托普利组、灸法Ⅰ+卡托普利组、灸法Ⅱ+卡托普利组、高血压对照组,另设正常对照组。经过10天治疗后,测量血压,并测定血浆中内皮素(ET)、一氧化氮(NO)。结果:高血压对照组的收缩压(SBP)、舒张压(DBP)明显高于正常对照组,各治疗组的SBP、DBP明显低于高血压对照组(P<0.01),各治疗组间则没有明显差异(P>0.05)。血浆NO含量各组间没有明显差异(P>0.05)。各治疗组与正常对照组的血浆中ET含量明显低于高血压对照组(P<0.01)。各治疗组ET/NO比值接近正常对照组(P>0.05)且明显低于高血压对照组(P>0.05)。结论:两种艾灸疗法有良好的降压作用,其降压机理与及纠正ET与NO的失衡状态有关。     

还原型谷胱甘肽在预防糖尿病大鼠勃起功能障碍中的研究

目的探讨还原型谷胱甘肽(GSH)在预防糖尿病大鼠勃起功能障碍中的作用。方法通过腹腔注射链脲佐菌素65mg/kg建立糖尿病大鼠模型,然后随机分成DM组和DM+GSH组,DM+GSH组每天肌肉注射GSH200mg/kg。10周后观察大鼠勃起功能,并获取海绵体组织检测其谷胱甘肽、一氧化氮合酶(NOS)与丙二醛(MDA)水平,用TUNEL法检测细胞凋亡。结果成功建立糖尿病大鼠模型。与未注射GSH的DM组相比,DM+GSH组和正常对照组(C组)勃起功能更好,勃起率分别是20%,62.5%和100%。GSH水平DM+GSH组和C组明显比DM组高,其3组含量每克蛋白分别是(75.83±15.62)、(61.47±8.65)和(35.03±12.29)mg(P<0.05);NOS水平在DM+GSH组每毫克蛋白为(133.9±31.9)U,与正常对照组每毫克蛋白为(142.2±31.2)U相当,但较DM组每毫克蛋白为(58.4±18.9)U高(P<0.05);MDA含量在DM组每毫克蛋白为(3.71±0.62)nmol,明显高于正常对照组和DM+GSH组(P<0.05),这两组每毫克蛋白为(2.08±0.34)nmol和(2.44±0.28)nmol;细胞凋亡率在DM组、DM+GSH组和C组的分别是(22.6±3.6)%、(10.8±1.7)%和(7.2±2.1)%(P<0.05)。结论还原型谷胱甘肽对糖尿病大鼠阴茎组织有较好的抗氧化作用,能减少细胞凋亡,对延缓糖尿病性ED的发生有一定的作用。     

肝硬化大鼠肝部分切除术后肝再生的干预研究

目的　以肝硬化大鼠为动物模型 ,研究药物对肝硬化大鼠肝部分切除术后肝再生的影响。方法　取健康的Wistar雄性大鼠 6 4只 ,以 6 0 ?l4油溶液 0 .3ml/ 10 0 g皮下注射 ,同时饮用 5 %酒精溶液 ,4 5d后制成肝硬化动物模型。模型大鼠随机分为 4组 ,16只 /组。全麻下均行左、中叶肝切除术。术后各组按以下方案处理 :A组 (对照组 )注射生理盐水 1mg/ (kg·d) ,B组为泮托拉唑组 ,注射 0 .2mg/ (kg·d) ,C组为重组人生长激素组 ,注射 0 .5U/ (kg·d) ,D组为两药合用组 ,同时给予泮托拉唑注射 0 .2mg/ (kg·d) ,重组人生长激素注射 0 .5U/ (kg·d) ) ,连续给药 1周。抽取静脉血样 ,取肝脏组织 ,检测肝功能、有丝分裂指数 (MI)、增殖细胞核抗原 (PCNA)、细胞核DNA含量。结果　泮托拉唑组、重组人生长激素组、两药合用组MI、PCNA阳性染色细胞量、细胞核DNA含量均高于对照组 (P <0 .0 5 ) ,两药合用组MI、PCNA阳性染色细胞量、细胞核DNA含量均高于泮托拉唑组、重组人生长激素组 (P <0 .0 5 ) ,但各组间肝功能变化无明显差异。结论　泮托拉唑组及重组人生长激素均对肝硬化大鼠肝部分切除术后肝细胞再生有促进作用 ,两药联合应用肝细胞再生更明显 ,其详细机制须待进一步研究。     

可溶性P-选择素对肝硬化门静脉高压术后门静脉血栓形成的影响

目的探讨可溶性P-选择素对肝硬化门静脉高压症术后门静脉血栓形成的影响。方法检测乙肝肝硬化患者在门静脉高压症围手术期血小板的数量及反映血小板功能的可溶性P-选择素水平的动态变化,比较其在有门静脉血栓形成组患者及无血栓形成组患者间的差异。结果血栓形成组患者及无血栓形成组患者间,血小板数量无显著差异,而可溶性P-选择素水平在术后第4～6天有显著性差异(P<0.05)。结论乙肝肝硬化患者在行门静脉高压症手术后,血小板功能的变化对门静脉血栓形成可能起着重要的作用。     

小干扰RNA干扰大鼠神经元Nogo受体mRNA表达的实验研究

目的观察大鼠Nogo受体(NgR)特异性小干扰RNA(small interfering RNA,siRNA)在原代神经元干扰其mRNA表达的效果。方法体外培养大鼠原代皮层和海马细胞,应用阳离子脂质体转染试剂转染4对化学合成的大鼠NgR特异性siRNA,72h后提取细胞总RNA,实时荧光定量RT-PCR检测NgR mRNA表达情况。结果4对siRNA均能够下调靶基因NgR的mRNA表达水平,siNgR199、siNgR562、siNgR772和siNgR964等干扰后,NgR mRNA的表达分别为对照siRNA干扰组的6.5%、62.4%、15.2%和6.86%,与对照siRNA干扰组比较有统计学意义(P<0.05)。结论化学合成的NgR特异性siRNA能够有效的干扰大鼠原代皮层和海马细胞内NgR基因mRNA的表达水平。     

Iron deficiency down-regulates the Akt/TSC1-TSC2/mammalian Target of Rapamycin signaling pathway in rats and in COS-1 cells

Iron deficiency (ID) is one of the most commonly known forms of nutritional deficiencies. Low body iron is thought to induce neurologic defects but may also play a protective role against cancer development by cell growth arrest. Thus, ID may affect cellular pathways controlling cell growth and proliferation, the mechanism of which is still not fully understood. The serine/threonine protein kinase Akt and its downstream target, the mammalian Target of Rapamycin (mTOR), is known to play a crucial role in the regulation of cell growth and survival. Therefore, we hypothesized that Akt/mTOR pathway could be influenced by ID. Three-week-old male Wistar-strain rats were divided into 3 groups and the 2 groups had free access to a control diet (C group) or an iron-deficient diet (D group). The third group (PF group) were pair-fed the control diet to the mean intake of the D group. After 4 weeks, rats were killed and their brains were sampled. In separate experiments, COS-1 cells were cultured with or without the iron chelator deferoxamine. Western blots of brain samples and COS-1 lysates were used to analyze the expression and phosphorylation state of Akt, TSC2, mTOR, and S6 kinase proteins implicated in the Akt/mTOR pathway. Using 2 different ID models, we show for the first time that iron deficiency depresses Akt activity in rats and in COS-1 cells, leading to a decrease in mTOR activity.