环孢霉素A致肝损伤

1例21岁男性患者,因肾病综合征(微小病变)服用环孢霉素A 100mg,2次/d,7d后,患者的ALT由24IU/L升至77IU/L,此时环孢霉素A血药浓度为70.25ng/mL,增加环孢霉素的给药剂量为125mg 2次/d,患者的ALT升至124IU/L,给予水飞蓟宾葡甲胺片100mg3次/d治疗后,转氨酶下降。     

环孢霉素A水性滴眼液的实验研制

目的实验研制环孢霉素A的水性滴眼液。方法使用增溶剂增加环孢霉素A的溶解度,用家兔做角膜移植后的抗免疫排斥试验。结果本法能有效增加环孢霉素A在水中的溶解度,抗免疫排斥的有效率90%。结论研制的水性滴眼液符合滴眼剂的要求,且药效优于油性滴眼液。     

环孢霉素A治疗坏死性巩膜炎的效果

目的 本文针对坏死性巩膜炎患者采用环孢霉素A治疗的效果进行研究分析.方法 收集本院自2015年1月～ 2015年12月这一期间收治的坏死性巩膜交患者5例(5眼)作为本次研究对象,对其采用环孢霉素A进行治疗,并对其进行为期3个月的追踪随访,观察其治疗效果.结果 经过环孢霉素A的治疗后,4例坏死性巩膜炎患者均已达到临床治愈标准,随访期间,患者均未出现复发情况.结论 针对坏死性巩膜炎患者采用环孢霉素A进行治疗具有较好的应用效果,可以使治愈率得到有效的提高,该方法值得在临床中大力的推广和应用.     

高效液相色谱法测定环孢霉素A滴眼液含量

目的建立测定环孢霉素A滴眼液含量的方法.方法采用高效液相色谱法,以环孢霉素D为内标,C8为固定相,乙腈-甲醇-水(552520)为流动相,检测波长为214 nm.结果环孢霉素A的平均回收率为99.7%,RSD为0.88%.结论本法简便、快速、准确.     

环孢霉素A的副作用及其临床监测

与其它药物一样,环孢霉素A也有许多副作用,主要是肾毒性和淋巴瘤。尚有肝功能损害、多毛症、牙龈增生等。骨髓移植患者还可出现高血压、液体潴留,儿童偶见惊厥。一般来讲、这些副作用较轻,与使用剂量有关。因此,对环孢霉素A的临床用量进行监测,即应用放射免疫方法(RIA)或高效液体层析(HPLC)测定环孢霉素A血清或血浆水平能使我们选择疗效较好而毒性最小的最佳用药剂量。     

高效液相色谱法测定环孢霉素A滴眼液含量

目的 建立测定环孢霉素A滴眼液含量的方法。方法 采用高效液相色谱法，以环孢霉素D为内标，C8为固定相，乙腈-甲醇-水(55：25：20)为流动相，检测波长为214nm。结果 环孢霉素A的平均回收率为99．7％，RSD为0．88％。结论 本法简便、快速、准确。     

高效液相色谱法测定环孢霉素A滴眼液含量

目的建立测定环孢霉素A滴眼液含量的方法.方法采用高效液相色谱法,以环孢霉素D为内标,C8为固定相,乙腈-甲醇-水(55:25:20)为流动相,检测波长为214 nm.结果环孢霉素A的平均回收率为99.7%,RSD为0.88%.结论本法简便、快速、准确.     

HPLC—MS法和mFPIA法测定全血环孢霉素A及其代谢物的比较

目的:对测定全血环孢霉素 A 的 HPLC-MS 法和单克隆荧光偏振免疫分析法(mFPIA 法)进行评价。方法:建立HPLC-MS 测定全血环孢霉素 A 及其代谢物的方法,采用多元线性回归对 HPLC-MS 法和 mFPIA 法测定的结果进行比较。结果:当患者肝、肾功能异常时,mFPIA 法测定结果同环孢霉素 A 及主要代谢物浓度呈线性相关,易导致检测结果偏高。结论:当患者肝、肾功能异常时,mFPIA 法不适宜作为环孢霉素 A 的临床监测方法。     

环孢霉素A联合方案治疗骨髓增生异常综合征-难治性贫血45例报告

目的 探讨环孢霉素A联合方案治疗骨髓增生异常综合征-难治性贫血(MDS—RA)疗效。方法 对45例MDS—RA应用环孢霉素A、康力龙、维甲酸治疗观察3-6月以上。结果 总有效率73．33％(33／45),基本缓解37．78％(17／45)，明显进步22．22％(10／45)，进步13．33％(6／45)，无效26．67％(13／45)。结论 环孢霉素A联合方案，对MDS-RA有一定疗效。     

低剂量环孢霉素A治疗难治型免疫性血小板减少症的疗效观察

目的观察低剂量环孢霉素A治疗难治型免疫性血小板减少症的疗效。方法将56例难治型免疫性血小板减少症患者随机分为对照组和观察组,每组28例。对照组采用大剂量地塞米松,观察组则采用低剂量环孢霉素A治疗。比较两组间治疗前后免疫状态。结果观察组患者痊愈率和总有效率显著高于对照组,两组间差异有统计学意义（P〈0.05）。治疗1、3个月后,观察组CD3＋、CD4＋/CD8＋显著高于对照组,CD8＋则显著低于对照组,两组间差异有统计学意义（P〈0.05）。结论低剂量环孢霉素A能有效抑制T细胞活性,对难治型免疫性血小板减少症具有很好的疗效。     

治疗帕金森病新药:腺苷A_(2A)受体拮抗剂

腺苷A2A受体在基底神经节选择性表达并与运动行为有关。流行病学研究和实验室研究均表明阻断腺苷A2A受体能减轻多巴胺能神经元的退行性病变。腺苷A2A受体拮抗剂在改善PD症状的同时还能减缓疾病的进程。因此,腺苷A2A受体拮抗剂很可能成为治疗PD的新药物。     

葛根黄豆甙元-PVP分散物的研究

本文采用聚乙烯吡咯烷酮(PVP)为载体,制备了葛根黄豆甙元固体分散物。经差热分析、X-射线衍射、偏光显微镜观察实验证明黄豆甙元-PVP 1∶9固体分散物为固体溶液或共沉淀物,其胶囊在人工胃液中最高累积释放百分量和人工肠液中平衡溶解度均是普通胶囊的8倍左右。     

SCH 58261: A selective A2A adenosine receptor antagonists

The recent discovery of selective antagonists for the A_2A adenosine receptors has been of great help to further research in this field. One compound, SCH 58261, 5- amino-7-(β-phenylethyl)-2-(8-furyl)pyrazolo[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine, is playing a key part in a variety of studies. This review describes its pharmacological characteristics as they are emerging in various laboratories. The compound has an affinity in the low nM range (Ki value of 1–2 nM) for A_2A receptors located on membranes from a variety of tissues and cell types, including rat and bovine brain striatum, human platelets, lymphocytes and neutrophils, porcine coronary arteries, and CHO cells transfected with the cloned human A_2A receptors. SCH 58261 has little or no affinity up to the μM range for adenosine A_2B, A₃, or other G protein-coupled receptors. Selectivity for A_2A vs. A₁ receptors varies from 53- to 750-fold, depending on membranes or type of assay. SCH 58261 blocks A_2A-receptor mediated increase of cyclic AMP formation with high potency (e.g., IC₅₀ values between 15 and 20 nM in human white blood cells). The tritiated form of SCH 58261 specifically labels A_2A receptors in discrete regions of the rat brain such as caudate-putamen, nucleus accumbens, and tuberculum olfactorium. In classic in vitro bioassays, such as A_2A-receptor-mediated vasodilation in coronary arteries, SCH 58261 displays competitive antagonistic properties (e.g., pA₂ value of 9.5 in porcine coronary arteries). In assays involving responses mediated by A₁ or A_2B receptors, SCH 58261 shows little or no activity up to concentrations about 100-fold higher than those affecting A_2A receptors (higher concentrations not being testable due to its poor water solubility). In the rat, SCH 58261 enhances locomotor activity (at 3.7 mg/kg ip), increases wakefulness (10 mg/kg ip) and slightly increases both blood pressure and heart rate (10 mg/kg ip). These activities appear to be specifically mediated by A_2A receptors since the drug counteracts the effect of A_2A receptor agonists in some experimental paradigms. In models mimicking CNS disorders, SCH 58261 potentiates the activity of L-DOPA or dopamine receptor agonists in the 6-hydroxydopamine-lesioned rat model. Moreover, the compound reduces brain infarct size in a rat model of cerebral ischemia. Altogether, SCH 58261 and its radiolabeled form have emerged as interesting tools for better understanding the function of A_2A receptors in physiological or altered conditions. Moreover, the neuroprotective properties of SCH 58261 indicate that drugs of this class have a potential for treatment of brain damage produced by Parkinson's disease or stroke. Drug Dev. Res. 42:63–70, 1997. © 1997 Wiley-Liss, Inc.     

Neurokinin A. A pharmacological study

Discovered in 1983, the decapeptide neurokinin A has been shown to occur in several peripheral organs and to exert a variety of biological effects. In this article, we review the most sensitive and selective in vivo and in vitro tests which have been used in various laboratories to evaluate naturally occurring or synthetic neurokinin A. A comparison of the effects of neurokinin A and those of its mammalian homologues, substance P and neurokinin B as well as those of tachykinins and related peptides is presented in the frame of a study directed toward characterization of neurokinin receptors. Indeed, neurokinin A has been shown to be particularly active on a neurokinin receptor subtype, the NK-2. Structure-activity studies performed with neurokinin A and its fragments as well as with several analogues of both the decapeptide and the heptapeptide NKA(4-10) have brought to the identification of the minimum structure required for activation of NK-2 receptors. Selective agonists for this receptor have been identified, in particular [Nle10]-NKA(4-10) and [beta-Ala8]-NKA(4-10).