抗坏血酸注射液对大鼠血小板粘附性的影响

本文用胶原粘附法测定了抗坏血酸注射液对大鼠血小板粘附性的影响。结果表明,抗坏血酸本身抑制血小板粘附性,而抗坏血酸注射液则轻度增强血小板粘附性,这与其所含稳定剂偏重亚硫酸钠明显增加血小板粘附性有关。     

不同PH值对抗坏血酸注射液稳定性的影响

本文在煮沸情况下作加速试验,考察不同 PH 值对5%抗坏血酸注射液的稳定性。     

注射用脉络通对在体兔纤维蛋白溶解活性及肺血栓溶解的药效学研究

为了验证注射用脉络通的药效学作用,用纤维蛋白平板法,进行了离体纤维蛋白溶解试验;用兔血浆优球蛋白溶解试验法,以溶解时间(ELT)为指标,进行了在体兔纤维蛋白溶解活性测定试验;用双缩脲法显色以吸光度为指标,进行了在体血浆纤维蛋白原含量测定试验;用125I标记血块注入兔静脉形成血栓法,以血中核素放射活性计数为指标,进行肺血栓溶解试验。结果表明,脉络通在离体条件下有溶解纤维蛋白和明显降低血浆纤维蛋白原含量的作用,并有一定的剂量效应关系,经t-检验在统计学上有非常显著的意义(P<0.01)。用药前各兔血液放射活性计数一般在700~900 cpm/g的范围内,静注脉络通后1 h受试物血液放射活性增加,有量效关系,在统计学上有非常显著的意义(P<0.01)。结论:注射用脉络通有加速优球蛋白溶解和降低血浆纤维蛋白原含量的作用,能够改善循环障碍,防治肺栓塞,是溶解血栓及预防血栓形成的有效药物。     

蛇毒纤维蛋白溶解酶综述

蛇毒中存在着能直接溶解纤维蛋白的酶类。对这类酶的深入研究,不仅有助于阐明蛇伤中毒的病理机制,而且为其应用开发提供了理论基础。自1976年Ouyang和Huang首次从尖吻蝮蛇毒中获得纯化的纤维蛋白溶解酶(以下简称纤溶酶)以来,迄今已从不同科属的至少15种蛇毒中获得了25种以上的纯化纤溶酶,并对其分子结构、酶学特性及其出血活性的关系进行了深入地研究。现就这些方面的研究进展作一简要综述。     

根霉菌产生血纤维蛋白溶解酶的研究

以一株具有高产血纤维蛋白溶解酶能力的菌株———中国根霉S2 8为出发菌株 ,通过对其培养基中的碳源、氮源、组成等进行研究 ,确定最佳培养基组成和培养条件     

根霉菌产生血纤维蛋白溶解酶的研究

以一株具有高产血纤维蛋白溶解酶能力的菌株－－中国根霉Ｓ２８为出发菌株,通过对其培养基中的碳源、氨源、组成等者研究,确定最佳培养基组成和培养条件。     

益母草注射液对家兔血液粘度及纤维蛋白原的影响

本文采用毛细管法和加热法观察了益母草注射液对家兔血液粘度及纤维蛋白原的影响。益母草注射液以16～48mg/kg剂量给药,使家兔血液粘度及纤维蛋白原降低,给药后12h降低作用最显著。     

原发性纤维蛋白溶解症(PF)1例报道

原发性纤维蛋白溶解症(简称原纤)是指由于某些原因,纤溶酶原被激活为纤溶酶,或纤溶酶抑制物减少,引起高纤溶酶血症,继后降解纤维蛋白原,水介其他血浆凝血因子,造成以低纤维蛋白原血症为主的低凝状态[1].临床表现为各种部位的严重出血.     

抗坏血酸氯化钠注射液的制备及质量控制

目的:制备100mL装量抗坏血酸氯化钠注射液并建立其质量控制方法。方法:以抗坏血酸为主药制备注射液;采用紫外-可见分光光度法测定其中主药的含量。结果:所制制剂检查、鉴别等均符合2005年版《中国药典》相关规定;抗坏血酸检测浓度的线性范围为4.0～12.0μg·mL-1(r=0.9999);平均回收率为99.85%(RSD=0.75%,n=6)。结论:本制剂组方合理,制备工艺简单可行,质量稳定可控。     

差示分光光度法测定抗坏血酸注射液含量

本文研究了 PH—差示分光光度法测定抗坏血酸注射液的含量。测定波庋为265nm,pH 选做6.2和2.0。样品回收率为99.94～100.02相对标准差小于0.32%。该法同碘量法比较无显著差异。     

偶合反应化学发光测定抗坏血酸的研究

本文基于 Fe(Ⅲ)氧化抗环血酸生成 Fe(Ⅱ)的反应和鲁米诺-氧-Fe(Ⅱ)化学发光反应相偶合.建立了流动注射化学发光法测定抗环血酸的新方法.该方法检出限为2×10~(-8)g/ml,RSD=2%(C=5×10g/ml n=11次)方法用于片剂中抗坏血酸的测定,取得满意结果。     

Effect of ascorbic acid status of the guinea pig on cadmium and zinc uptake from the intestine

Intestinal uptake of cadmium and zinc was studied in vitro by a tissue accumulation method in latent chronic scorbutic guinea pigs and in animals given excessively large amounts of vitamin C. The results indicated that the ascorbic acid (AA) status of the animals had no effect on intestinal uptake of zinc or cadmium.     

Lack of correlation between lysosomal enzyme activity and ascorbic acid content in brain of lead-treated animals

The administration of lead acetate increased acid phosphatase activities in the rat brain and four regions (cerebral cortex, diencephalon plus mesencephalon, pons plus medulla, and cerebellum) of the guinea pig brain, whereas ascorbic acid content in the brain of these animals remained unchanged following lead administration. Acid phosphatase activity also showed an increase in scorbutic guinea pig brain. Lipid peroxidation facilitated by ascorbic acid in the cerebral lysosome fraction of rat was not affected by lead. These results suggest that ascorbic acid is not directly concerned with the alteration in acid phosphatase activity induced by lead treatment.     

两种辅料对地塞米松磷酸钠注射液中杂质的影响

目的:分析对比依地酸二钠与亚硫酸氢钠对地塞米松磷酸钠注射液中杂质的影响.方法:建立地塞米松磷酸钠注射液杂质Ⅰ(C22 H30 FNa2 O11 PS)的定量分析方法,以杂质Ⅰ、地塞米松的含量和总杂质的峰面积占比来评价制剂的安全性.结果 与结论:以依地酸二钠为辅料的地塞米松磷酸钠注射液中杂质Ⅰ含量更低,总杂质也相对更少.     

Pharmacokinetics of ascorbic acid in man

Summary The pharmacokinetic characteristics of ascorbic acid have been investigated in normal adult volunteers, using a two-compartment open model. After oral administration in a normal gelatine capsule the bioavailability of ascorbic acid was 69%. It was 98% when a sustained-release preparation was given in an identical capsule. During daily oral intake of ascorbic acid 1 g in the sustained-release form blood levels reached the equilibrium state within 3 days. Daily doses of ascorbic acid 1 g resulted in tissue saturation in 7 days, with a profound change in the pharmacokinetics of the vitamin. The binding of ascorbic acid to plasma proteins was low (24%). Its significance for the pharmacokinetic behaviour of the drug is discussed.     

Effect of ascorbic acid supplementation on nitric oxide metabolites and systolic blood pressure in rats exposed to lead

Background:

Extended exposure to low levels of lead causes high blood pressure in human and laboratory animals. The mechanism is not completely recognized, but it is relatively implicated with generation of free radicals, oxidant agents such as ROS, and decrease of available nitric oxide (NO). In this study, we have demonstrated the effect of ascorbic acid as an antioxidant on nitric oxide metabolites and systolic blood pressure in rats exposed to low levels of lead.

Materials and Methods:

The adult male Wistar rats weighing 200-250 g were divided into four groups: control, lead acetate (receiving 100 ppm lead acetate in drinking water), lead acetate plus ascorbic acid (receiving 100 ppm lead acetate and 1 g/l ascorbic acid in drinking water), and ascorbic acid (receiving 1 g/l ascorbic acid in drinking water) groups. The animals were anesthetized with ketamin/xylazine (50 and 7 mg/kg, respectively, ip) and systolic blood pressure was then measured from the tail of the animals by a sphygmomanometer. Nitric oxide levels in serum were measured indirectly by evaluation of its stable metabolites (total nitrite and nitrate (NOχ)).

Results:

After 8 and 12 weeks, systolic blood pressure in the lead acetate group was significantly elevated compared to the control group. Ascorbic acid supplementation could prevent the systolic blood pressure rise in the lead acetate plus ascorbic acid group and there was no significant difference relative to the control group. The serum NOχ levels in lead acetate group significantly decreased in relation to the control group, but this reduction was not significantly different between the lead acetate plus ascorbic acid group and the control group.

Conclusion:

Results of this study suggest that ascorbic acid as an antioxidant prevents the lead induced hypertension. This effect may be mediated by inhibition of NOχ oxidation and thereby increasing availability of NO.     

Role of calcium in isoproterenol cytotoxicity to cultured myocardial cells

Primary cultures of rat myocardial cells were used to evaluate the cellular dynamics of calcium accumulation after exposure to isoproterenol (ISO). Non-toxic concentrations of ISO (2.4 × 10^?7 M) caused a gradual increase in myocyte calcium uptake. These effects peaked 3 min after exposrue and returned to control levels within 2 min. Toxic concentrations of ISO caused a biphasic increase in calcium uptake. The initial phase peaked 1 min after exposure and returned to control levels by 3 min. A second phase was characterized by a progressive increase in calcium uptake that plateaued 10 min after exposure. Ascorbic acid (AA, 5 × 10^?3 M) and sodium bisulfite (SB, 9.6 × 10^?4 M) did not modify the calcium uptake of the initial phase, whereas propranolol (1 × 10^?6 M) and verapamil (1 × 10^?5 M) prevented the initial rise in calcium uptake. In contrast, the antioxidants prevented the second phase of ISO-induced calcium uptake, whereas verapamil and propranolol did not. The toxic accumulation of calcium induced by ISO may be due to oxidative damage of the sarcolemma. Antioxidants may prevent the formation of oxidative metabolites from ISO and the subsequent calcium overload. Our results show that agents which modify slow calcium-channel transport do not prevent ISO-induced calcium overload in our cell culture system.     

多巴胺受体激动剂对乙醇引起大鼠纹状体抗坏血酸释放的影响

目的　研究多巴胺受体激动剂对乙醇引起大鼠纹状体抗坏血酸 (AA)释放的影响。方法　应用脑内透析技术结合高效液相电化学检测的方法。结果　乙醇 (3 0 g·kg-1,ip)显著增加纹状体抗坏血酸释放 ,高于基础水平的 2 0 0 %左右。多巴胺D1受体激动剂SKF 38393(10mg·kg-1,ip)对纹状体AA释放及乙醇引起纹状体AA释放均无显著影响。多巴胺D2 受体激动剂LY 1715 5 5 (0 5 ,1 0mg·kg-1,ip)显著增加纹状体AA释放及乙醇引起纹状体AA释放 ,但LY1715 5 5与乙醇对纹状体抗坏血酸释放的增加没有协同作用。具有多巴胺D1受体强拮抗剂和D2 受体强激动剂特性的溴隐亭 (10mg·kg-1,ip)在给药后 6 0min内对纹状体AA释放及乙醇引起纹状体AA释放均有显著的增加作用 ,且两者有协同作用。非选择性多巴胺受体激动剂阿扑吗啡也能增加纹状体AA释放及乙醇引起纹状体AA释放 ,而 0 2mg·kg-1的阿扑吗啡与乙醇有协同作用 ,0 4,0 8mg·kg-1的阿扑吗啡与乙醇没有协同作用。结论　多巴胺D2 受体的兴奋参与调节纹状体AA的释放 ,兴奋D2 受体同时抑制D1受体能够协同乙醇引起的大鼠纹状体抗坏血酸释放的作用。     

高效液相色谱法测定氨酪酸氯化钠注射液中的α-吡咯烷酮

目的建立高效液相色谱法检测氨酪酸氯化钠注射液中α-吡咯烷酮含量的方法标准。方法选用CAPCELL PAK C18柱为色谱柱;流动相采用p H2.1的磷酸二氢钾溶液-甲醇（90：10）;流速维持在1.0m L/min;紫外检测波长设定为210nm;柱温为30℃;进样量为10μL。结果α-吡咯烷酮浓度为0.4-5.0mg/L时其线性关系良好,r=0.9998,平均回收率为100.27%（RSD=0.54%,n=6）。结论本研究建立的HPLC法对于氨酪酸氯化钠注射液中的α-吡咯烷酮测定效果良好且方便快捷。