康妇宁栓中苦参、黄芩、蛇床子的薄层鉴别

采用薄层色谱法对康妇宁栓中苦参、黄芩、蛇床子三味中药材进行定性鉴别,斑点清晰,重现性好。苦参:用2%NaOH溶液制备的硅胶G薄层板,以苯-丙酮-甲醇(8∶3∶0.5)为展开剂,展开,晾干,再以甲苯-醋酸乙酯-甲醇-水(2∶4∶2∶1)10℃以下放置后的上层溶液为展开剂,喷改良碘化铋钾试液-无水乙醇(2∶1)显色。黄芩:采用聚酰氨薄膜,以乙酸为展开剂,于紫外灯(275nm)下检视。蛇床子:硅胶G-0.5%CMC-Na薄层板,以苯-醋酸乙酯(30∶1)为展开剂,置紫外光灯(365nm)下检视。上述分析方法简便、快速、准确,为康妇宁栓的质量评价方法提供了定性依据。     

僵蚕薄层鉴别方法的改进

目的：改进中药材僵蚕的薄层鉴别的方法。方法：甲醇溶解，超声提取，氯仿-甲醇（12：1）展开，365nm紫外灯下检视。结果：对照药材图谱中有清晰的红色荧光斑点，无阴性干扰。结论：该方法操作简单，斑点清晰，重现性好，可用于不同来源僵蚕药材的鉴别及利咽灵片中僵蚕药材的检测。     

牛黄消炎片、妇乐颗粒中掺入土大黄的鉴别方法研究

目的建立TLC、HPLC法鉴别牛黄消炎片、妇乐颗粒中是否掺入土大黄。方法采用TLC法,硅胶G板,醋酸乙酯-丁酮-甲酸-水(10∶7∶1∶1)为展开剂,在365 nm下检视;采用HPLC法,Lichrospher C18(250 mm×4.6 mm,5μm),乙腈-甲醇-水(7∶30∶63)为流动相,检测波长为320 nm。结果土大黄苷在365 nm下显持久的蓝紫色荧光斑点,高效液相色谱法中呈现色谱峰。结论鉴别法简便、快速、专属性强,能有效地检查牛黄消炎片、妇乐颗粒是否掺入土大黄苷。     

薄层色谱—分光光度法测定黛芩化痰丸中靛玉红和黄芩甙含量

本文用薄层色谱一分光光度法测定黛芩化痰丸中靛玉红和黄芩甙含量,靛玉红的分析是在硅胶G薄层板上,用苯-醋酸乙酯-甲酸-水(60:20:1.00:10)为展开剂,分离的斑点以氯仿提取,用550 nm波长测定吸收度,计算含量。回收率为98.01％,变异系数为1.3％。黄芩甙的测定是在硅胶GF_254薄层板上,用正丁醇-乙酸-水(4:1.5:4.2)为展开剂,分离的斑点用紫外分析仪定位后,以甲醇-水(9:11)提取,用276.0nm波长测定吸收度,计算含量。回收率为100.9％,变异系数为0.94％。     

咽炎糖浆的制备及质量控制

目的：对咽炎糖浆进行薄层色谱鉴别，为该药确定质量标准。方法：分别以氯仿-甲醇-水(40：10：1)，醋酸乙酯甲酸-冰醋酸-水(30：2：2：4)为展开剂，对咽炎糖浆中牛蒡子和甘草进行定性实验。结果：分离良好，斑点清晰。结论：方法简便可靠，重现性好。     

肝豆片质量标准改进研究

目的 增加对肝豆片处方中药材质量控制方法,全面提高肝豆片质量标准,更有效地控制产品的质量。 方法 建立高效液相色谱法对处方中君药大黄进行含量测定,并对处方中臣药黄连、金钱草建立薄层色谱鉴别方法。 结果 黄连鉴别以甲苯-异丙醇-乙酸乙酯-甲醇-水(6∶1.5∶3∶1.5∶0.5)为展开剂,以浓氨水作为饱和溶液,置紫外灯365 nm下检视;金钱草鉴别以甲苯-甲酸乙酯-甲酸(10∶8∶1)为展开剂,以3%三氯化铝乙醇溶液为显色剂,置紫外灯365 nm下检视;大黄含量测定大黄素在8.48～25.44 mg·L-1的浓度范围,峰面积A与浓度C呈现良好的线性关系,相关系数为0.999 4,回收率为95.8%,RSD=0.8%(n=6)。 结论 方法准确、快速、重现性好,质量标准得到改进。     

成方中黄连、黄柏的薄层鉴别的研究

目的 探讨采用薄层色谱法鉴别几种成方制剂中黄连，黄柏成份的效果。方法 采用硅胶G为吸附剂，以正丁醇—冰醋酸—水(7：1：2)为展开剂，紫外光灯(365nm)下检视。结果 黄连对照药材显3个亮黄色的荧光斑点，黄柏对照药材显两个亮黄色的特征荧光斑点。结论 本方法可以用于鉴别制剂中黄连成份。     

二次薄层色谱—荧光法测定培坤胶囊中橙皮苷含量

建立了培坤胶囊中橙皮苷的二次薄层色谱—荧光分析法。即先以醋酸乙酯 -甲醇 -水 (10 0∶ 17∶13)展开 ,再以甲苯 -醋酸乙酯 -甲醇 -水 (2 0∶ 10∶ 1∶1)上层溶液展开 ;荧光测定条件为λex=310 nm,λem=510 nm。该法可有效地排除共存组分的干扰 ,并提高检测的灵敏度。橙皮苷在 1μg～ 11μg范围具有良好的线性 ,r =0 .9977。     

抗菌消炎胶囊中土大黄苷的薄层鉴别及HPLC鉴别方法研究

目的 建立抗菌消炎胶囊中土大黄苷的快速检验方法.方法 采用薄层色谱法快速检验样品中的土大黄苷,以乙酸乙酯-丁酮-水(10∶7∶1)为展开剂,在紫外光灯(365 nm)下观察斑点荧光,并用高效液相色谱法确证.结果 土大黄苷有非常清晰的蓝紫色荧光,正品制剂在相应位置上无斑点;土大黄苷液相色谱主峰在325 nm有最大吸收.结论 本法操作简便、快速、准确.     

薄层扫描法测定阴道栓中盐酸小檗碱的含量

目的:建立阴道栓中盐酸小檗碱的含量测定方法。方法:以苯-醋酸乙酯-异丙醇-甲醇-水(6∶3∶1. 5∶1. 5∶0. 3)为展开剂,在紫外灯(365nm )下检视,另在薄层扫描仪上扫描,检测波长为430nm。结果:盐酸小檗碱进样量在0. 25μg～1 .25μg范围内线性关系良好(r=0. 9987) ,平均回收率为97 .63 % (RSD=1 .88 % )。结论:本方法简便、准确,可用于该制剂的质量控制。     

氟哌啶醇季铵盐衍生物抑制氯化钾所致大鼠主动脉平滑肌细胞内钙浓度增加

目的:动态观察氟哌啶醇季铵盐衍生物(F_3)对血管平滑肌细胞内钙浓度的影响。方法:利用激光共聚焦显微镜动态观察F_3(0.o1-10μmol/L)对由KCl(30mmol/L)诱导的大鼠血管平滑肌细胞钙荧光强度增加的作用。结果:KCl可诱发细胞内钙荧光强度迅速增强,F_3可以拮抗由KCl诱导的细胞内钙荧光强度增强作用,并呈量效依赖性和时间依赖性,终强度(KCl:67±24;F_3 0.o1μmol/L:57±13;0.1μmol/L:40±13;1μmol/L:29±9;10μmol/L:20±6)。在加入F_3后,钙荧光强度的变化最快时程是在给F_3后0-30s。结论:F_3拮抗血管收缩主要是由于阻断了Ca~(2 )通道。     

不同训练时段影响甲基苯丙胺诱导的大鼠自身给药行为的形成

目的 观察不同时间给予甲基苯丙胺(METH)对大鼠形成自身给药行为的影响。方法 通过6 d的FR1程序训练合格的大鼠进入实验。按照4个给药时间8:00-8:30,10:00-10:30,11:30-12:00及16:00-16:30和2个给药因素生理盐水和METH 0.05 mg·kg^-1分为8组,持续8 d。在自身给药装置中FR1程序记录给药次数和有效鼻触和无效鼻触次数。结果 与同一给药时间的溶剂对照组相比,METH组大鼠自身给药的次数及有效鼻触次数显著增加(P<0.05)。不同时间段给予METH组的给药次数和有效鼻触次数均没有显著性差异,但是从8 d的给药次数来看,分别为8:00-8:30组(86.2±23.8)<10:00-10:30组(104.3±41.3)<11:30-12:00组(123.4±50.3)<16:00-16:30组(155.0±51.7)。从前4 d给药时间8:00-8:30改为后4 d给药时间11:30-12:00后,给药次数和有效鼻触次数明显增加(P<0.05);从前4 d给药时间11:30-12:00改为后4 d给药时间8:00-8:30后,给药次数和有效鼻触次数明显减少(P<0.05)。8组大鼠间无效鼻触次数没有显著差异。结论 10:00-17:00时间段进行训练有利于大鼠自身给药行为的形成。     

Hemodynamic effects of intravenous administration of olprinone hydrochloride on experimental pulmonary hypertension

To examine acute effects of olprinone hydrochloride (CAS 106730-54-0, Coretec) on pulmonary hypertension, hypoxic pulmonary hypertension was produced in 6 adult Beagle dogs. Using this pulmonary hypertension model, single intravenous bolus injections of olprinone at doses of 10, 30 and 100 micrograms/kg were administered at 5-min intervals and hemodynamic parameters were evaluated. Heart rate increased at doses of 30 and 100 micrograms/kg, but did not change at a dose of 10 micrograms/kg. Mean aortic pressure, mean pulmonary arterial pressure, pulmonary vascular resistance and systemic vascular resistance and right ventricular stroke work index did not change at doses of 10 and 30 micrograms/kg, but they decreased significantly at a dose of 100 micrograms/kg. On the other hand, cardiac index and the first derivative value of the left ventricular pressure did not show significant change at all doses. These results indicate the vasodilating effects on peripheral and pulmonary vessels in hypoxic model at high doses of olprinone. Its application in right heart failure accompanied by pulmonary hypertension therefore is expected to yield promising results.     

Dose-proportional pharmacokinetics of a methylphenidate extended-release capsule

OBJECTIVE: To assess the dose-proportionality of the 10 mg, 20 mg and 30 mg methylphenidate extended-release (MPH ER) capsule formulations in healthy adults. MATERIALS: Metadate CD (methylphenidate HCl, USP) extended-release capsules (10, 20 and 30 mg) were obtained from Celltech Manufacturing Inc. (Rochester, NY, USA). METHODS: This was a single-center, single-dose, fasted, randomized, open-label, 3-way crossover study with a 1-week washout period between doses, in 24 healthy male and female subjects, aged 21-40 years. MPH plasma concentration-time data were used to calculate the pharmacokinetic parameters for each treatment. The 20 mg capsule, the first FDA-approved dosage strength, was used as reference treatment. RESULTS: Twenty-three subjects completed all 3 study periods. Regardless of the dose, MPH ER capsules exhibited similar PK profiles as evidenced by a biphasic absorption profile, consisting of a sharp initial increase followed by a second increase in MPH plasma levels, all occurring at the same times. All 90% confidence intervals for the 10:20 mg and 30:20 mg dose-normalized geometric mean ratios were within the 80-125% FDA limits for bioequivalence. This was true for Cmax (maximum observed concentration), AUC(0-last) (area under the plasma concentration curve from time 0 to the last measurable time point) and AUC(0-inf) (area under the plasma concentration curve from time 0 to infinity). Adverse events were mild and the number and types of adverse events experienced by subjects did not differ among the 3 dosages. CONCLUSION: Data collected from this study demonstrate the dose proportionality of the new 10 mg and 30 mg dosage strengths of MPH ER capsules with the 20 mg capsule. The availability and predictability of these dosage strengths should facilitate dose titration of ADHD patients.     

Characterization of muscarinic cholinergic receptors in intact myocardial cells in vitro.

Muscarinic acetylcholine receptors (mAChR) were studied on heart cells grown in culture by the radioligand binding technique. We used [3H]n-methyl-scopolamine to monitor the level of receptors on intact cardiocytes. The number of mAChR was very low during the first days in culture (23 fmol/dish). It increased gradually until it reached a plateau on the 4th day (180 fmol/dish), where it remained for 1-2 weeks. To determine whether contractile activity affected the level or affinity of mAChR, the cardiocytes were exposed to agents that stimulate or arrest the heart beat. Treatment with triiodothyronine (T3, 10-90 nM) for 48 hr caused a reduction in the level of the receptors by 20-30% without changing significantly the affinity of the receptors. Similarly, electrical stimulation caused a reduction in the level of the receptors by 30-40%, without a significant influence on creatine kinase activity. When the myocardial cells were treated with Ca-channel blocker such as metoxyverapamil (D600) (10-30 micrograms/mL) or diltiazem (10-25 micrograms/mL) the level of the receptors was also reduced by 30-40%. The reduction in the receptor binding sites was accompanied by an increase in Kd from 0.8 to 3.2 nM in D600-treated cells, whereas there was no significant change in the radioligand affinity after application of diltiazem. Treatment with D600 or T3 together with cycloheximide showed that under these experimental conditions the rate of receptor degradation was accelerated. The half-life of the receptors in the control was 27 hr, whereas the half-lives of T3 and D600 were 15 and 18 hr, respectively. It is concluded that regulation of the amount of cholinergic receptors occurs at the level of receptor breakdown, and simple linkage does not exist between the rate of cardiac contractions and the number of mAChR.     

血卟啉注射液的稳定性

目的:研究血卟啉注射液不同温度放置条件下的稳定性。方法:采用高压液相色谱法(HPLC),色谱柱PolarlsC18A柱(5μm,4.6mm×250mm),检测波长390nm,流动相:甲醇∶水∶乙腈∶四氢呋喃(160∶220∶105∶190),每1000mL流动相加入磷酸0.5mL调节pH值,流速:1.5mL·min-1。结果:血卟啉注射液随温度升高(30～70℃)含量呈直线下降,在温度30,40,50,60℃下降50%的时间分别为100,28,7,3d。在4℃4mo,30℃5d内未见明显变化。结论:由于血卟啉注射液对温度敏感,建议贮放条件应在30℃下不超过5d。     

Effects of intravenous magnesium sulfate on the QT interval in patients receiving ibutilide

STUDY OBJECTIVE: To determine the effect of intravenous magnesium sulfate on the QT and QTc intervals in patients receiving ibutilide for immediate chemical cardioversion of atrial flutter or fibrillation. DESIGN: Prospective, randomized, double-blind, placebo-controlled trial. SETTING: Hospital cardiology unit. PATIENTS: Twenty patients (mean age 72 +/- 14 yrs) with atrial fibrillation (12 patients) or atrial flutter (8 patients) who were scheduled to receive ibutilide. INTERVENTION: After determining that the patients' baseline QTc intervals were less than 440 msec and baseline serum magnesium levels were within normal limits (mean 2.1 +/- 0.29 mg/dl), the patients were randomly assigned to receive either a 10-minute infusion of magnesium sulfate 2 g in 50 ml of 0.9% sodium chloride or placebo immediately before ibutilide therapy. An additional 2 g of intravenous magnesium sulfate or placebo was given over 1 hour, 10 minutes after the first dose of ibutilide. MEASUREMENTS AND MAIN RESULTS: QT interval duration was measured manually in all 12 leads by using a 0.5-mm-scale precision ruler and magnifying lens. The QT interval increased 29% from baseline at 30 minutes after ibutilide therapy in the placebo group (p=0.007), but no significant change from baseline occurred in the magnesium sulfate group. The 30-minute QTc interval in the placebo group was 18% higher than the baseline value (p=0.01) but did not change significantly in the magnesium sulfate group. QTc changes from baseline were greater in the placebo group than in the magnesium sulfate group at 30 minutes (75 vs 19 msec, respectively, p=0.04). Magnesium sulfate reduced the risk of an ibutilide-induced QTc interval increase of greater than 30 msec or greater than 60 msec and reduced the risk of a QTc interval value of more than 500 msec by 65%, 60%, and 68%, respectively (p=0.07, p=0.175, and p=0.160). CONCLUSIONS: Prophylactic administration of intravenous magnesium sulfate prevents increases in the QT and QTc interval 30 minutes after the last infusion of ibutilide.     

Calcium antagonists stimulate prostaglandin synthesis by cultured rat cardiac myocytes and prevent the effects of hypoxia

The effect of three calcium antagonists on the synthesis of prostacyclin (PGI2, assayed as 6-Keto-PGF1 alpha) and PGE2 by cultured rat cardiac myocytes and fibroblasts was investigated. In myocytes only, bepridil, diltiazem and verapamil (10(-9) to 10(-7) M) stimulated PGs synthesis by two- to three-fold, dose-dependently. At a concentration of 10(-6) or 10(-5) M the intensity of the stimulation of PGI2 and PGE2 decreased. Cobalt chloride (2 X 10(-3) M) did not change PGs synthesis (pg/mg of protein/30 min; means +/- SE, N = 10; PGE2: 365 +/- 59 and 463 +/- 89 treated vs controls; PGI2: 824 +/- 214 and 799 +/- 143 treated vs controls). After 30 min exposure of myocytes to hypoxic conditions (glucose-free medium and low PO2), the glycogen content was half that of the controls (P less than 0.001), ATP content did not change and PGI2 and PGE2 synthesis increased (X1.5, P less than 0.05). When applied to myocytes 30 min before inducing hypoxia, the three calcium antagonists stimulated PGs synthesis by three- to seven-fold at maximal effect, and bepridil (10(-8) M) or diltiazem (10(-7) M) prevented the hypoxia-induced decrease in glycogen content. With 10(-5) M drug concentration, the effect on PGs was not significant, except for the effect of bepridil on PGI2 (P less than 0.05). It is concluded that therapeutic concentrations of calcium antagonists simultaneously prevent the decrease in myocyte glycogen induced by hypoxia and stimulate PGs synthesis by myocytes.     

High frequency of highly active antiretroviral therapy modifications in patients with acute or early human immunodeficiency virus infection

STUDY OBJECTIVES: To examine the frequency of highly active antiretroviral therapy (HAART) modifications, the reasons for these modifications, and toxicities of these drugs in patients receiving their first HAART regimen after a diagnosis of acute (< 2 mo from infection) or early (2-12 mo) human immunodeficiency virus (HIV) infection. PATIENTS: Fifty-one patients who were enrolled in the Acute Infection and Early Disease Research Program at a Baltimore, Maryland, site between January 1, 1998, and April 30, 2002, and who chose to start HAART. MEASUREMENTS AND MAIN RESULTS: Time from initiation of therapy to first modification-defined as change in any HAART drug without an interruption in therapy or as simultaneous discontinuation of all drugs within the regimen-and time from initiation of therapy to reinitiation of therapy were recorded, as well as reasons for modification and reinitiation. With a median follow-up of 1,549 days, 21 (41%) of 51 patients received HAART continuously, but only 10 (20%) continued to receive their original regimen without any modification. Among the 41 patients (80%) who received modified therapy, the main reasons for the first modification were toxicity (16 patients), nonadherence (8), and new data on treatment efficacy or safety (8). Of 30 patients who stopped HAART, 18 restarted HAART at a later time. CONCLUSION: The high frequency of treatment modification among patients treated after acute or early HIV infection underscores the importance of determining the usefulness of antiretroviral therapy early in HIV infection, and the need for more tolerable regimens if HAART is to be started at this stage.     

GABAB receptors play a role in the development of tolerance to ethanol in mice

RATIONALE: There is evidence that drugs that improve or impair learning can facilitate or block ethanol tolerance, respectively. Since GABA(B) receptors have been shown to be involved in processes related to learning, it is possible that this system could play a role in the development of rapid tolerance to ethanol. OBJECTIVES: The aim of this study was to verify the influence of one GABA(B) agonist and two GABA(B) antagonists on tolerance to the effect of ethanol on motor coordination. METHODS: Male Swiss mice were trained on a continuously accelerating rota-rod device. Animals were pretreated with the GABA(B) agonist (-)-baclofen (3, 5, or 7 mg kg(-1)) or saline, 30 min before ethanol (1.75 g kg(-1)), and were tested 5, 10, and 15 min later on the rota-rod. In another set of experiments, mice were pretreated with the GABA(B) antagonists CGP36742 (1, 3, 10, or 30 mg kg(-1)) or CGP56433 (0.1, 0.3, 1.0, or 3.0 mg kg(-1)), or saline, 30 min before the test under ethanol. Rapid tolerance was evaluated 24 h after the first ethanol injection, by injecting all animals with ethanol and retesting them on the rota-rod. RESULTS: The results showed that (-)-baclofen (5 mg kg(-1)) significantly (ANOVA + Tukey's test) blocked rapid tolerance, whereas CGP36742 (3 and 10 mg kg(-1)) and CGP56433 (0.3, 1, and 3 mg kg(-1)) facilitated rapid tolerance in a dose-dependent way. The blockade of rapid tolerance by (-)-baclofen was antagonized by previous administration of CGP36742 or CGP56433. CONCLUSIONS: The current results suggest that rapid tolerance to ethanol is subjected to inhibition by a GABAergic GABA(B) receptor-mediated system in the mouse.