交流示波极谱法测定盐酸氯丙嗪及其制剂的含量

用交流示波极谱法测定盐酸氯丙嗪及其制剂的含量，不用指示剂，从极谱图形的变化指示终点。其优点为操作简单、快速，结果准确、直观。     

盐酸氯丙嗪注射液细菌内毒素检查法的实验研究

目的 研究盐酸氯丙嗪注射液对细菌内毒素检查实验的干扰情况，并建立其细菌内毒素检查的质量标准。方法 参照《中国药典》2005年版二部附录XIE细菌内毒素检查法进行实验．应用两个生产厂家的鲎试剂对两个厂家的盐酸氯丙嗪注射液进行干扰试验研究。结果 盐酸氯丙嚷注射液对细菌内毒素检查有干扰作用，但通过盐酸三羟甲基氨基甲烷（Tris）缓冲液（pH7．2）稀释可消除干扰。结论 该制剂可以用细菌内毒素检查法（凝胶法）代替兔热原检查法控制其产品质量。     

盐酸氯丙嗪片的质量分析

本文通过对36批盐酸氯丙嗪片的质量进行分析，评价了盐酸氯丙嗪片的整体质量情况。     

光照影响盐酸氯丙嗪注射液质量的考察

对盐酸氯丙嗪注射液质量受光照影响进行了考察,得出随着光照强度的增强其颜色逐步加深,pH值逐步下降,氧化产物的吸收值逐步升高,含量则逐步下降。     

光和热对盐酸氯丙嗪注射液稳定性的影响

目的 研究盐酸氯丙嗪注射液在光和热作用下的稳定性.方法 采用恒温加速试验和高温光照试验进行考察.结果 高温条件下,盐酸氯丙嗪注射液的降解符合一级动力学规律;光照条件下,符合零级动力学规律.结论 光照下提高温度可增大降解速率,降解速率的大小与波长有关.     

糖衣对盐酸氯丙嗪片含量测定的影响

目的:研究糖衣对盐酸氯丙嗪片含量测定的影响。方法:采用紫外分光光度法。先取空白糖衣溶液在200～400nm波长范围内进行紫外扫描,再分别对4个厂家的样品经剥糖衣和不剥糖衣处理后在254nm波长处测定吸光度并计算含量,并将数据进行配对设计的t检验。结果:空白糖衣溶液在200～400nm波长范围内无吸收;剥糖衣和不剥糖衣处理后样品含量测定结果无显著性差异(P>0.05)。结论:糖衣不影响盐酸氯丙嗪片的含量测定结果,盐酸氯丙嗪片可不剥糖衣进行含量测定。     

高效液相色谱法测定盐酸氯丙嗪注射液的含量

目的 采用高效液相色谱测定盐酸氯丙嗪注射液的含量.方法 采用C18(4.6 mumx 250 mm5 μm)色谱柱;流动相:0.1 mol/L磷酸二氢钾(用磷酸调节pH 3.0)-乙腈(55∶45);检测波长254 nm;流速:1.0 ml/min;进样量:20μl;柱温:35℃.结果 在该色谱条件下,盐酸氯丙嗪在4.99～49.91μl/ml范围内呈良好的线性关系,(r =0.9999,n=8).结论 所建立的方法灵敏、准确、简便,可作为盐酸氯丙嗪注射液的含量测定方法.     

盐酸氯丙嗪注射液的HPLC测定

采用苯基键合硅胶柱经ＨＰＬＣ测定盐酸氯丙嗪注射液的含量，平均回收率１００．１３％，ＲＳＤ为０．８５％。     

高效液相色谱法测定安乃近氯丙嗪注射液中盐酸氯丙嗪含量

目的 采用高效液相色谱法测定安乃近氯丙嗪注射液的含量.方法 采用C18色谱柱(250 mm×4.6 mm,5μm),流动相为0·1 mol/L磷酸二氢钾(用磷酸调节pH:3.0)-乙腈(55:45),检测波长254 nm,流速1.0 mL/min,进样量20μL,柱温35℃.结果 盐酸氯丙嗪质量浓度在4.99-49.91μg/mL范围内与峰面积呈良好线性关系,r=0.9999(n=8).结论 所建立的方法灵敏、准确、简便,可作为安乃近氯丙嗪注射液的含量测定方法.     

HPLC法测定盐酸氯丙嗪片的含量

目的：建立HPLC法测定盐酸氯丙嗪片的含量。方法：HypersilBDSClB色谱柱（250mm×4．6mm，5μm），流动相为甲醇-2．0mol·L-1庚烷磺酸钠溶液（15：85，用冰醋酸调节pH至3．0），柱温为25oC，流速为1．0ml·min-1，检测波长为254nm。结果：盐酸氯丙嗪在50～200μg·ml-1的浓度范围内与峰面积呈线性关系（r=0．9996），平均回收率为99．8％，RSD为0．5％（n=9）。结论：该法专属性强，操作简便，结果准确。     

HPLC法测定盐酸氯丙嗪片的含量

目的建立测定盐酸氯丙嗪片含量的方法。方法采用HPLC法,C8柱(250mm×4.6mm,5μm);流动相为乙腈-0.5%三氟醋酸(用四甲基乙二胺调节pH值至5.3)(50︰50);检测波长为254nm。结果盐酸氯丙嗪在3.29～49.35μg/mL浓度范围内线性关系良好(r=0.9996),平均回收率为99.00%,RSD=0.43%。结论本方法简便、快速、准确,专属性强,可作为盐酸氯丙嗪片的含量测定方法。     

Effect of chlorpromazine on the interaction between phasic and tonic electrocortical arousal mechanisms

The effect of chlorpromazine on the rate of habituation of phasic arousal responses has been studied in cats carrying permanently implanted cortical recording electrodes. In the sleeping animal repeated presentation of an auditory stimulus (1 sec duration, 3000 Hz) at intensities which only produced a localised, phasic electrocortical change in the auditory cortex, resulted in the rapid habituation of this latter response. Once habituation had occurred the intensity of the stimulus was increased until a similar change in electrocortical activity once again appeared in the auditory cortex. The habituation procedure was then repeated. In this way it was possible to habituate the animal gradually to successively higher intensities of auditory stimulation without ever inducing behavioural arousal or tonic, generalised changes in electrocortical activity. Indeed, it was possible to reach a level of stimulation which previously would have induced overt behavioural effects and tonic arousal. It may be concluded that alterations in the activity of the mechanisms responsible for phasic electrocortical responses leads to changes in the responsiveness of the animal even during sleep.Following chlorpromazine phasic electrocortical responses were still elicited but their rate of habituation was significantly increased. Thus the overall effect of chlorpromazine was a marked shortening in the time taken to train the animal while still asleep, not to respond behaviourally or with tonic electrocortical changes to a particular auditory stimulus.     

Effect of clonidine and chlorpromazine on centrally evoked electrodermal responses and their interaction with yohimbine

Both clonidine and chlorpromazine reduced the amplitude of electrodermal responses (EDR) evoked by stimulation of the hypothalamus at a constant submaximal frequency (10–16 Hz). The ED₅₀ for clonidine was approximately 5 μg/kg and that for chlorpromazine was about 1 mg/kg. Yohimbine pretreatment (0.5 mg/kg, i.v.) antagonized the effects of clonidine but did not alter the effectiveness of clorpromazine in inhibiting these responses. Yohimbine alone was without effect on these sympathetic-cholinergic responses. These results suggest that clonidine and chlorpromazine depress central sympathetic reactivity by different mechanisms.     

毛细管区带电泳电化学检测人体尿样中的双氯灭痛、氯丙嗪

目的建立毛细管区带电泳法测定人体尿样中双氯灭痛、氯丙嗪含量的方法。方法采用弹性石英毛细管（31.5cm,25μmi.d.,360μmo.d.）,以4.90×10-3mol/LNa2HPO4-7.80×10-3mol/LNaH2PO4（pH=7）为缓冲液,10kV分离电压,5kV电渗进样10s,碳纤维电极工作电极（长200μm,直径8μm）,检测电势0.72V。结果双氯灭痛、氯丙嗪两种药物分别在9.90×10-6～5.00×10-4mol/L（r=0.9982）、5.0×10-7～1.0×10-4mol/L（r=0.9998）范围内表现出良好的线性,其回收率分别为104%,96.0%。结论该方法简便、快速、准确,可作为人体尿样中双氯灭痛、氯丙嗪的分离检测方法。     

盐酸氯丙嗪鼻黏膜用药和穴位注射治疗顽固性呃逆疗效比较

目的比较盐酸氯丙嗪鼻黏膜用药和足三里穴位注射两种给药方式治疗顽固性呃逆的效果。方法将70例顽固性呃逆患者随机分成鼻黏膜用药组和穴位注射组。鼻黏膜用药组35例给予盐酸氯丙嗪滴鼻,12.5mg（双侧总量）/次,4次/d;穴位注射组35例给予盐酸氯丙嗪足三里穴位注射,25mg（双侧总量）/次,2次/d。两组疗程均为3d。结果鼻黏膜用药组和穴位注射组总有效率分别为97.1%和91.4%,经统计学处理,两组差异无统计学意义（P〉0.05）。结论盐酸氯丙嗪注射液两种给药方式治疗顽固性呃逆均有较好的疗效。其中鼻黏膜用药方式具有简便、速效和无痛苦的特点,更易于为患者所接受。     

盐酸芦氟沙星的电化学行为研究

目的研究盐酸芦氟沙星(rufloxacin hydrochloride,简称RUFX)的电化学行为和电极反应机理,拟定了测定RUFX的吸附伏安法.方法用单扫示波极谱法、循环伏安法和直流极谱法等多种技术进行研究.结果在KH2PO4-Na2HPO4(pH7.00)底液中,RUFX在汞电极上有一线性扫描还原峰,峰电位Ep=-1.27V(vs.Ag/AgCl),该峰具有明显的吸附性.吸附粒子为RUFX中性分子,测得RUFX在汞电极上的饱和吸附量为5.51×10-11mol/cm2,每个RUFX分子所占电极面积为3.01nm2,RUFX在悬汞电极上的吸附符合Frumkin等温式.测得吸附系数β=7.74×105,电子转移数(n)为2,不可逆吸附的电子转移系数(α)为0.76,表面电极反应的速率常数ks=0.23/s.建立了吸附伏安法测定RUFX的最佳条件,检出限为1.0×10-9mol/L.结论证实该体系为具有吸附性的不可逆过程.     

Electrochemical behavior and square wave voltammetric determination of doxorubicin hydrochloride

The electrochemical behavior of doxorubicin hydrochloride was investigated by cyclic voltammetry (CV) and square wave voltammetry (SWV). From CV and SWV studies of doxorubicin hydrochloride in the acetate buffers of various pH values, it was found that protons were involved in the reduction of the antibiotic at the H+/e- ratio at one (deltaEp/pH = -53 approximately -61 mV at 23 degrees C), proposing the electrochemical reduction of the quinone moiety in its anthraquinone aglycone. Its electrochemical behavior was pseudo-reversible in the acetate buffer of pH 3.5 by exhibiting the well-defined single cathodic and anodic waves and the ratio of Ip(a)/Ip(c) at approximately one over the scan rates of 10 approximately 100 mV/s. Fast and sensitive SWV showing a single peak of doxorubicin has been applied for its quantitative analysis using an acetate buffer of pH 3.5. A linearity was obtained when the peak currents (Ip) were plotted against concentrations of doxorubicin in the range of 5.0 x 10(-7) M approximately 1.0 x 10(-5) M with a detection limit of 1.0 x 10(-7) M.     

Effect of metabolites of chlorpromazine on plasma prolactin levels in male rats

Since prolactin secretion is under vigorous dopaminergic inhibition, neuroleptic drugs can, because of their capacity to block dopamine receptors, produce large increases in plasma prolactin levels in man and laboratory animals. The capacity of intramuscular (i.m.) chlorpromazine and 6 of its metabolites to increase plasma prolactin levels in male rats was compared. 7-Hydroxychlorpromazine produced increases in plasma prolactin equivalent to those produced by chlorpormazine. The following metabolites had no effect on plasma prolactin levels after i.m. injections of 5 mg/kg: 8-hydroxychlorpromazine; 7, 8-dihydroxychlopromazine; 8-hydroxy-7-methoxychlorpromazine; 7-methoxychlorpromazine; and chlorpromazine sulfoxide. 8-Hydroxychlorpromazine, 7-methoxychlorpromazine, 7, 8-dihydroxychlorpromazine and chlorpromazine sulfoxide had no effect even after 25 mg/kg i.m. The capacity to increase rat plasma proclactin correlates highly with other methods of determining potential antipsychotic activity of chlorpromazine and its derivatives.     

HPLC with electrochemical detection to measure chlorpromazine,thioridazine and metabolites in human brain

Thirteen phenothiazine compounds were separated chromatographically using high performance liquid chromatography with coulometric electrochemical detection. These could be extracted from brain tissue using direct homogenization in tetrahydrofuran followed by one centrifugation, evaporation of supernatant and reconstitution in water. Fluphenazine was used as the internal standard. The absolute lower limit of detection was approximately 50 pg/mg wet tissue, and recovery rates for most standards added to brain homogenates were greater than 85%. Chromatograms from patients receiving chlorpromazine (600 mg) and thioridazine (600 mg) are shown and endogenous brain levels quantified. The results are discussed with respect to their relevance in schizophrenic research.     

盐酸氯丙嗪联合帕洛诺司琼预防化疗药物致恶心呕吐的临床观察

目的探讨盐酸氯丙嗪联合帕洛诺司琼预防化疗药物致恶心呕吐的临床疗效.方法 2014年1月—2014年7月在襄阳市中心医院行高致吐性化疗药物的住院患者126例,随机分为对照组和治疗组,每组63例.对照组患者在化疗第1天,开始化疗前30 min静脉滴注盐酸帕洛诺司琼注射液,0.25 mg/次,1次/d,注射时间30 s以上.治疗组在对照组基础上肌肉注射盐酸氯丙嗪注射液25 mg/次.3周为1个化疗周期,两组在1个化疗周期后观察恶心、呕吐的控制率.结果对照组和治疗组急性呕吐控制率分别为76.19%、84.13%,延迟性呕吐控制率分别为50.79%、63.49%,治疗组急性、延迟性呕吐控制率均显著高于对照组,两组比较差异具有统计学意义(P<0.05).对照组和治疗组急性恶心控制率分别为58.73%、77.78%,延迟性恶心控制率分别为 49.21%、65.08%,两组比较差异具有统计学意义(P<0.05).对照组和治疗组急性食欲减退控制率分别为87.30%、90.48%,延迟性食欲减退控制率分别为84.12%、87.30%,两组比较差异无统计学意义.结论 盐酸氯丙嗪联合帕洛诺司琼预防化疗药物致恶心呕吐具有较好的临床疗效,且不会增加不良反应,值得临床推广应用.