反卷积分法研究长春西汀推拉式渗透泵控释片体内外相关性

目的：采用反卷积分法评价长春西汀渗透泵控释片的体外释放与Beagle犬体内吸收相关性。方法：以0．5％SDS水溶液为溶出介质，测定长春西汀的体外释放度；高效液相色谱测定犬体内血药浓度，选择长春西汀普通片为参比制剂，应用反卷积分法评价长春西汀推拉式渗透泵体内体外相关性。结果：体外累计释放度（Y）与输入函数（R）回归方程为iY=237．99R-13．544（r=0．9763），表明长春西汀推拉式渗透泵体内体外相关性良好。结论：反卷积分法适合自制长春西汀推拉式渗透泵控释片体内外相关性研究。     

长春西丁包合物的制备和体外溶出度考察

 目的制备长春西丁(VIN)包合物,对其体外溶出度进行考察。方法测定长春西丁在不同浓度枸橼酸(CA)和环糊精(CD)水溶液中的溶解度;选用β-环糊精(β-CD)和羟丙基-β-环糊精(HP-β-CD),分别采用研磨法(KE)、旋转蒸发法(CE)和冷冻干燥法(FD)制备了VIN/CD和VIN/CD/CA包合物;按照中国药典2000年版二部附录桨法对包合物中药物溶出度进行考察。结果VIN溶解度随CA浓度的升高而线性增加;药物在CD水溶液中的相溶解度曲线呈现典型的A_L型;制备方法对药物的体外溶出行为有影响;采用CE或FD法制备的VIN/CD/CA包合物比相应的VIN/CD包合物表现出更令人满意的体外药物溶出行为,它能明显提高药物在水中的溶解度和溶出速度;VIN/CD/CA包合物中,CD种类和用量对药物溶出行为无显著影响。结论对于生物碱类难溶性药物,在包合物中加入酸性辅料(如枸橼酸)可以显著降低增溶同等用量药物所需的环糊精的用量,近而减低生产成本,减小制剂服用体积。     

长春西汀在治疗眼外伤玻璃体切除术后的应用

目的：探讨眼外伤玻璃体切除术后应用长春西汀改善微循环的疗效。方法：选择我院2009-01/2011-12眼球钝挫伤患者92例92眼,行玻璃体切除术后随机分为两组,治疗组46例46眼,对照组46例46眼。治疗组应用长春西汀注射液静点20mg,1次/d,连续14d。观察期为1,3,6mo及末次随访（最长12mo）,以视力作为观察指标。结果：随访3mo后,治疗组视力明显高于对照组（P〈0.05）。结论：眼外伤玻璃体切除术后应用长春西汀,可以提高患者的视力。     

长春西汀对突发性耳聋患者的疗效分析

目的：分析临床使用长春西汀治疗突发性耳聋患者的疗效。方法：选取2009年9月—2014年1月间诊治的突发性耳聋患者64例,将其随机分为对照组及治疗组（各组32例）,对照组患者予银杏达莫,静脉滴注;治疗组患者给予长春西汀,静脉滴注,两组患者均予加用激素及腺苷钴胺和高压氧协助治疗,10 d为一个疗程,比较两组患者的疗效。结果：治疗组患者耳聋治疗的总有效率为87.50%,对照组患者的总有效率为62.50%,经比较其差异有统计学意义（P〈0.05）;治疗组患者耳鸣的有效率为84.37%,对照组耳鸣的有效率为62.50%（P〈0.05）。结论：长春西汀可改善内耳循环,用于突发性耳聋的治疗,其疗效较为满意,不良反应较少。     

长春西汀治疗椎-基底动脉供血不足60例疗效观察

目的:观察长春西汀治疗椎-基底动脉供血不足(VBI)的临床疗效及安全性。方法:120例VBI患者随机分为治疗组和对照组各60例。治疗组用长春西汀注射液20 mg加生理盐水250 ml静脉滴注,1次/天,共14 d;对照组用灯盏花素注射液40 mg加生理盐水250 ml静脉滴注,1次/天,共14 d。结果:治疗组总有效率93.33%,明显高于对照组70.00%(P0.01)。2组患者治疗后血流动力学和血液流变学指标较治疗前均有明显改善(P0.01),且治疗组均优于对照组(P0.01),2组未见明显不良反应。结论:长春西汀治疗VBI疗效确切,值得临床推广。     

长春西汀注射剂中有关物质定位的数字化研究

目的：用相对保留时间（RRT）的方式定位长春西汀注射剂4个已知杂质。方法：考察长春西汀4个杂质的RRT对不同的色谱仪、试剂、色谱柱及色谱条件的耐用性,确定理想的色谱方法。结果：确定流动相0．2mol·L^-1醋酸铵溶液-乙腈（40：60）（pH6．83）及不同品牌的5根色谱柱,杂质a,d,b,c和主成分的RRT分别为0．4,0．66,0．78,0．87和1。结论：通过对此方法的耐用性考察,探讨了杂质对照品定位数字化的影响因素和应对方法,希望对今后标准研究工作具有一定的借鉴作用。     

Omeprazole does not change the oral bioavailability or pharmacokinetics of vinpocetine in rats

Previous studies proved that food strongly enhanced the bioavailability of vinpocetine. Food may change the pharmacokinetics of a drug by affecting various factors, including gastrointestinal pH. However, the influence of proton pump inhibitor-induced pH alterations on vinpocetine pharmacokinetics is not known. The aim was to evaluate the influence of omeprazole on the pharmacokinetics of oral vinpocetine. One group of male Wistar rats received single oral doses of vinpocetine (2 mg/kg - regimen V). In the second group, omeprazole (10 mg/kg) was administered intraperitoneally for 5 days before vinpocetine administration (regimen OV). For analysis of vinpocetine pharmacokinetics, blood samples were obtained before and 0.25, 0.5, 1, 1.5, 2, 3, 4, 5, 6, 8, 10 and 12 h after vinpocetine administration. Vinpocetine concentrations were measured by high performance liquid chromatography (HPLC). The mean values of AUC(0-t), AUC(0-inf) and C(max) in regimen V were very similar to respective values in regimen OV. The mean T(max) in both regimens was estimated for 1.5 h. There were no statistically significant differences between both regimens. In conclusion, omeprazole did not affect the pharmacokinetic profile of vinpocetine.     

Role of vinpocetine in cerebrovascular diseases

A cerebrovascular accident, or stroke, is defined as the abrupt onset of a neurological deficit, which can be due to ischemia. Cerebral ischemia is caused by a reduction in blood flow that thereby decreases cerebral metabolism. Chronic cerebral hypoperfusion leads to irreversible brain damage and plays an important role in the development of certain types of dementia. Vinpocetine, chemically known as ethyl apovincaminate, is a vinca alkaloid that exhibits cerebral blood-flow enhancing and neuroprotective effects. Non-clinical and clinical studies have suggested multiple mechanisms responsible for the beneficial neuroprotective effects of vinpocetine. As no significant side effects related to vinpocetine treatment have been reported, it is considered to be safe for long-term use. This vasoactive alkaloid is widely marketed as a supplement for vasodilation and as a nootropic for the improvement of memory. The present review focuses on studies investigating the role of vinpocetine in cerebrovascular diseases.     

补肾益气活血法治疗短暂性脑缺血发作临床观察

[目的]观察补肾益气活血法治疗短暂性脑缺血发作的临床疗效。[方法]将60例随机分为两组,对照组30例采用常规西药治疗,治疗组30例在常规西药治疗基础上加用补肾益气活血汤口服,两组均连续用药7d,观察临床疗效。[结果]两组在3d内控制率和治疗总有效率有非常显著性差异(P<0.01);两组治疗7d后,治疗组总有效率86.67%,对照组总有效率73.33%,临床疗效治疗组优于对照组(P<0.05)。[结论]补肾益气活血汤治疗短暂性脑缺血发作疗效显著。     

Early ethanol exposure and vinpocetine treatment alter learning‐ and memory‐related proteins in the rat hippocampus and prefrontal cortex

This study investigates the effects of early exposure to ethanol on cognitive function and neural plasticity‐related proteins in the rat brain. Sprague‐Dawley rats were administered 12% ethanol solution (4 g/kg/day i.p.) or saline from P4 to P9. Vinpocetine, a phosphodiesterase type 1 inhibitor, was tested to determine whether it could reverse any changes induced by early ethanol exposure. Hence, from P25 to P31, ethanol‐exposed male rats were injected with vinpocetine (20 mg/kg/day i.p.) or vehicle (DMSO) prior to undergoing behavioral testing in the open field and Morris water maze (MWM) tests. Ethanol exposure did not adversely affect spatial memory in the MWM. A key finding in this study was a significant ethanol‐induced change in the function of the phosphorylated extracellular signal‐related kinase (P‐ERK) signaling pathway in the prefrontal cortex (PFC) and dorsal hippocampus (DH) of rats that did not display overt behavioral deficits. The P‐ERK/ERK ratio was decreased in the PFC and increased in the DH of ethanol‐exposed rats compared with controls. Rats that received vinpocetine in addition to ethanol did not display any behavioral changes but did show alterations in neural plasticity‐related proteins. Mitogen‐activated protein kinase phosphatase was increased, whereas brain‐derived neurotrophic factor was decreased, in the PFC of vinpocetine‐treated ethanol‐exposed rats, and phosphorylated‐glycogen synthase kinase β and synaptophysin were increased in the DH of these rats. This study provides insight into the long‐term effects of early ethanol exposure and its interaction with vinpocetine in the rat brain. © 2016 Wiley Periodicals, Inc.