反相离子对梯度洗脱色谱法测定甲麻芩苷那敏片中3组分含量

目的:建立测定甲麻芩苷那敏片中3组分(盐酸甲基麻黄碱、黄芩苷和马来酸氯苯那敏)含量的反相离子对HPLC法。方法:采用色谱柱Inertsil ODS-3(250mm×4.6mm,5μm,柱温30℃),以[0.2%辛烷磺酸钠溶液-三乙胺(100∶0.2,磷酸调节pH至4.3)]-甲醇(50∶50)为流动相A,以甲醇为流动相B,流动相B的比例由1%~98%匀速递增进行洗脱;检测波长为215nm;流速为1.0mL/min。结果:盐酸甲基麻黄碱、黄芩苷及马来酸氯苯那敏的线性范围分别为0.5~25μg(r=0.9998),0.3~17μg(r=1.000)和0.01~0.5μg(r=1.000),平均回收率分别为100.3%(RSD=1.3%)、99.9%(RSD=1.1%)和99.6%(RSD=1.2%)。结论:本文建立的方法简单、迅速,可用于甲麻芩苷那敏片中3组分的含量测定。     

马来酸桂哌齐特治疗急性脑梗死的临床分析

目的探讨马来酸桂哌齐特注射液(商品名克林澳)治疗急性脑梗死(ACI)的临床疗效。方法将64例急性脑梗死患者随机分为两组,两组患者除给予常规治疗外,治疗组32例给予克林澳320mg为主治疗,加入生理盐水250ml静脉滴注,每日一次；对照组32例(即治疗方法之一)给予川芎嗪0．2g 胞二磷胆碱1．0g为主治疗,加入生理盐水250ml静脉滴注,每日一次。两组患者均治疗两周,观察治疗前后临床疗效和纤维蛋白原、凝血酶原时间的生化指标进行对比分析。结果治疗组显效率68．7％,对照组显效率34．4％,两组基本痊愈和显效比较有明显差异(P<0．05),且治疗组血浆纤维蛋白原明显降低(P<0．05)。结论马来酸桂哌齐特注射液治疗急性脑梗塞疗效肯定,能明显改善神经功能的损伤。减少了并发症和后遗症的发生,是一种安全有效的药物。     

马来酸曲美布汀治疗功能性消化不良疗效观察

目的观察马来酸曲美布汀治疗功能性消化不良（FD）的临床疗效。方法选择FD患者64例，随机分为对照组和治疗组各32例。治疗组给予马来酸曲美布汀200mg口服，1日3次；对照组给予谷维素10mg口服，1日3次．疗程2周。观察治疗前后症状变化。结果马来酸曲美汀对嗳气有效率为84．6％、恶心有效率为86．7％、腹胀有效率为81．2％、腹痛治疗有效率为90．4％、腹泻有效率为84．6％、便秘有效率为85．7％，总体评估总改善率为82％。无明显不良反应。结论马来酸曲美汀治疗FD是安全有效的。     

小儿酚氨咖敏颗粒含量测定方法改进研究

提高小儿酚氨咖敏颗粒含量测定质量标准,更有效的控制其含量.用HPLC法同时测定氨基比林、对乙酰氨基酚和咖啡因的含量.采用Diamonsal C18色谱柱,流动相为乙腈-0.05mol·L-1磷酸二氢钾溶液-三乙胺-磷酸(10∶90∶0.02∶0.03)(调节pH值为3.5),流速为1ml·min-1,检测波长215nm.线性关系与回收率氨基比林0.06～1.80μg(r=0.9999),101.22%(RSD=0.45%);对乙酰氨基酚0.075～2.25μg(r=0.9999),101.27%(RSD=0.51%);咖啡因0.02～0.6μg(r=0.9999),100.7%(RSD=0.70%).方法简便,准确,重现性好.     

HPLC法同时测定复方锌布颗粒中马来酸氯苯那敏和布洛芬的含量

目的建立同时测定复方锌布颗粒中马来酸氯苯那敏和布洛芬的含量的方法。方法采用Alltech C18(250 mm×4.6 mm,5μm)色谱柱,以乙腈-醋酸钠缓冲液(醋酸钠6.13 g,加水750 ml使溶解,用冰醋酸调节pH至4.0)-异丙醇(50∶45∶5)为流动相,流速1.0 ml.min-1,检测波长263 nm。结果马来酸氯苯那敏、布洛芬线性范围分别为31.65~84.4、2254.65~6012.4μg.ml-1,平均回收率分别为99.42%和99.06%。结论本方法可快速准确地检测复方锌布颗粒中的马来酸氯苯那敏和布洛芬。     

渗透促进剂对马来酸噻吗洛尔角膜透过性的影响

目的：研究渗透促进剂对马来酸噻吗洛尔（TM）角膜透过性的影响。并对其刺激性进行评价。方法：使用双室扩散池方法测定加入6种渗透促进剂后离体兔眼角膜对TM透过量的变化。以角膜水化值和眨眼值频率为指标评价渗透 促进剂的体内外刺激性。结果：0．05％的去氧胆酸钠和1％的泊洛沙姆188分别使TM的表现透过系数增大1．88和1．55倍而未见体内外刺激性。进一步提高泊洛沙姆188浓度抑制药物透过角膜。月桂氮Zhuo酮虽能显著增加TM的透过量却对角膜组织造成损伤。结论：低浓度的去氧胆酸钠和泊洛沙姆188为刺激性小、有效的眼用渗透促进剂。     

高效液相色谱法测定糖浆剂中扑尔敏与伪麻黄碱的含量

采用高效液相色谱法测定了抗感冒糖浆剂中扑尔敏与伪麻黄碱的含量。方法以扑热息痛做内标，扑尔敏的回收率为９９．４３％（ｎ＝５），伪麻黄碱的回收率为９９．６４％（ｎ＝５）。     

HPLC法测定复方敏立通片中各组分的含量

采用反相ＨＰＬＣ法，以醋酸氟氢松为内标，在氰基柱上以水—甲醇—乙腈—三乙胺（８０∶２０∶２０∶１．４，用磷酸调整ｐＨ为７．５）为流动相，检测波长为２５４ｎｍ，同时测定复方敏立通片中马来酸氯苯那敏和倍他米松的含量．方法简便，快速准确，各组分与内标有良好线性关系和分离度．平均回收率马来酸氯苯那敏为９９．２％（ＲＳＤ＝０．７％），倍他米松为１００．９％（ＲＳＤ＝０．６％），ｎ＝７．     

A comparative study on the effects of alpha-hexachlorocyclohexane and its metabolite beta-pentachlorocyclohexene on growth and monooxygenase activities in rat liver

The present study adds support to the hypothesis that β-pentachlorocyclohexene (β-PCH) is a primary intermediate in α-hexachlorocyclohexane (α-HCH)4 metabolism in the rat. Degradation of α-HCH to β-PCH was shown to occur in vitro and in vivo, partially by non-enzymic catalysis. β-PCH accumulated in liver and adipose tissue of α-HCH treated rats, which had received the glutathione-lowering agent diethyl maleate. β-PCH disappears from the body much more rapidly than the parent compound α-HCH: about 50 per cent of a single i.p. dose were degraded within 2.5 hr, while half-life of α-HCH is known to be approximately 130 hr. To maintain equimolar liver concentrations, β-PCH must be given in doses 100-fold higher than α-HCH. β-PCH and α-HCH were fed for a period of ten days at various dose levels to give steady-state liver concentrations. It was found that β-PCH has similar hepatic effects to α-HCH: both agents induced liver growth and a phenobarbital-type pattern of monooxygenase activities, as measured by the following substrates: aminopyrine, ethylmorphine, benzphetamine, 4-nitroanisole, aniline, benzo[α]pyrene, ethoxyresorufin and 2,5-diphenyl-oxazole. Threshold doses for these effects were 30–43 μmoles/kg/day for β-PCH and 1.0–1.7 μmoles/kg/day for α-HCH. However, on the basis of molar hepatic concentrations β-PCH was a more potent inducer than α-HCH (2–10 times). Threshold concentrations ranged from 0.4 to 0.6 nmoles β-PCH/g liver and from 0.7 to 1.5 nmoles α-HCH/g liver. β-PCH concentrations in livers of rats treated even with high doses of α-HCH were below the threshold for induction of liver growth and of monooxygenase increases. It is, therefore, highly unlikely that β-PCH is responsible for the effect of α-HCH on rat livers.