Differential effects of the pyrethroid tetramethrin on tetrodotoxin-sensitive and tetrodotoxin-resistant single sodium channels

The differential effects of the pyrethroid tetramethrin on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) single sodium channel currents in rat dorsal root ganglion (DRG) neurons were investigated using the outside-out configuration of patch-clamp technique. Channel conductances were 10.7 and 6.3 pS for TTX-S and TTX-R sodium channels, respectively, at a room temperature of 24–26°C. The single-channel current of TTX-S sodium channels at the test potential of −30 mV was −1.27 ± 0.25 pA, and was not changed after exposure to 10 μM tetramethrin (−1.28 ± 0.23 pA). The open time histogram of TTX-S single-channel currents could be fitted by a single exponential function with a time constant of 1.27 ms. After exposure to 10 μM tetramethrin, the open time histogram could be fitted by the sum of two exponential functions with time constants of 1.36 ms (τ_fast) and 5.73 ms (τ_low). The percentage of contribution of each component to the population was 62% for the fast component representing the normal channels and 38% for the slow component representing the tetramethrin modified channels. The amplitudc of TTX-R single-channel currents was slightly changed from −0.72 ± 0.14 to −0.83 ± 0.07 pA by 10 μM tetramethrin. The open time histogram of TTX-R single-channel currents could be fitted by a single exponential function with a time constant of 1.92 ms. In the presence of 10 μM tetramethrin, the open time histogram could be fitted by the sum of two exponential functions with time constants of 2.07 ms (τ_fast) and 9.75 ms (τ_slow). The percentage of contribution of each component was 15% for the fast, unmodified component and 85% for the slow, modified component. Differential effects of tetramethrin on the open time distribution of single sodium channel currents explains the differential sensitivity of TTX-S and TTX-R sodium channels.     

抑制剂对酪氨酸酶影响的初步研究

采用酶动力学及聚丙烯酰胺凝胶电泳方法研究了ＮａＨＳＯ３、ＮａＮ３、ＫＳＣＮ、ＤＤＣ对酪氨酸酶的抑制作用。ＮａＨＳＯ３、ＮａＮ３、ＫＳＣＮ为非竞争性抑制作用，随着抑制剂浓度增加，酶活性逐渐减弱。当ＮａＨＳＯ３、ＮａＮ３、ＫＳＣＮ的浓度分别达到１．２ｍｍｏｌ／Ｌ１２。５ｍｍｏｌ／Ｌ１２．５ｍｍｏｌ／Ｌ时，酶活性的抑制率为１００％、５０％、２４％。ＤＤＣ对酪氨酸酶的抑制作用为竞争性抑制作用，其浓度达４ｍｍｏｌ／Ｌ时，酶活性１００％受到抑制。     

示波极谱滴定法测定盐酸苯海拉明苯妥英钠及其制剂含量

采用示波极谱滴定法测定了盐酸苯海拉明、苯妥英钠及其制剂含量,所得结果均达到药典标准,与非水滴定法或提取后分光光度法比较,本法具有快速、准确、简单、操作方便、免用有机溶剂的优点。     

白芍总苷治疗口腔扁平苔藓的疗效评价研究

目的：观察羟氯喹及羟氯喹与白芍总苷两者合并治疗口腔扁平苔藓（OLP）的疗效,并且同时比较两种定性疗效评价方法,对OLP的损害程度和治疗效果进行评价。方法：随机选取两组初诊患者,分别采用羟氯喹及羟氯喹与白芍总苷治疗三个月,使用绝对数值标准和相对变化标准分别计算。结果：白芍总苷和羟氯喹联合用药,对OLP糜烂型和充血型损害有效。单用羟氯喹治疗OLP糜烂型和充血型损害无效。对于OLP斑纹型损害,两组均有效。白芍总苷和羟氯喹联合用药治疗OLP,可以减少羟氯喹的不良反应。采用＂绝对数值标准＂的定性评价方法与采用＂相对变化标准＂的定性评价方法相比,具有记录简便、评价准确的优点。结论：白芍总苷辅助治疗口腔扁平苔藓有效;绝对数值标准高效准确。     

高碘摄入对SD大鼠钠/碘同向转运体蛋白表达影响的免疫组化研究

目的:动态观察长期高碘摄入对SD大鼠甲状腺细胞钠/碘同向转运体(NIS)蛋白表达的影响.方法:SD大鼠分别饲以去离子水及不同碘浓度的碘化钾水,给碘后1 d及1,2,4,8周处死.测定尿碘、组织碘含量,免疫组织化学方法观察甲状腺细胞NIS蛋白表达水平.结果:高碘摄入可引起甲状腺滤泡细胞膜表面NIS蛋白表达的下降.短期较低浓度的高碘摄入对NiS蛋白的表达无明显影响,而较高浓度的碘摄入则引起NIS蛋白表达的明显减少;长期高碘摄入对NIS蛋白表达的抑制作用,可在机体自我调节机制作用下得以部分恢复,但NIS蛋白表达仍处较低水平.结论:高碘摄入可导致甲状腺细胞表面NIS蛋白表达下降,随摄碘浓度的增加抑制作用增强;不同浓度的碘摄入对NIS蛋白表达的抑制作用表达时间不同.     

高危出血患者应用吉派林抗凝血液透析疗效观察

目的：观察危重型肾功能衰竭合并高危出血患者选择抗凝药物进行血液透析治疗的效果。方法：应用吉派林(低分子肝素钠)作为抗凝剂进行血液透析。结果：129例病人进行血液透析386次，均没有出血发生。结论：吉派林在高危出血患者血液透析中使用方便，安全，效果良好。     

硝普钠治疗急性心肌梗塞并发泵衰竭(附28例疗效分析)

本文总结了用硝普钠治疗AMI并发泵衰竭28例临床资料。根据治疗前左心功能和血压水平,分组讨论其剂量与疗程;并将不同程度泵衰竭对硝普钠的疗效分组列表,进行了统计学处理。结果:有效率85.7%;在无血流动力学监测的条件下,只要严密观察临床指标,应用硝普纳同样可行。     

头孢哌酮钠在醋酸钠平衡液中的稳定性

考察了头孢哌酮钠在醋酸钠平衡液中的稳定性。二药配伍后，置室温（２５℃）及３７℃水浴中，６ｈ内溶液无颜色改变，亦无沉淀、气体产生，头孢哌酮钠均在初始浓度的９５％以上。     

丙戊酸钠与尼莫地平治疗偏头痛的疗效比较

目的：观察丙戊酸钠与尼莫地平治疗偏头痛的疗效有否差别。方法：偏头痛１２９例，随机分为丙戊酸钠治疗组６６例（男性１７例，女性４９例；年龄２５±ｓ７ａ），丙戊酸钠开始剂量为０．２ｇ，ｐｏ，ｔｉｄ，以后根据发作频率及程度逐渐增量，最大量１．４ｇ／ｄ，共用３ｍｏ；尼莫地平对照组６３例（男性１８例，女性４５例，年龄２７±６ａ），尼莫地平３０ｍｇ，ｐｏ，ｔｉｄ，共用３ｍｏ。结果：丙戊酸钠组总有效率为８３％。尼莫地平组为８５％，２组无明显差异（Ｐ＞０．０５）．未见严重不良反应。结论：丙戊酸钠与尼莫地平治疗偏头痛安全有效、疗效相似。     

Interaction of Nucleoside Analogues with the Sodium–Nucleoside Transport System in Brush Border Membrane Vesicles from Human Kidney

The therapeutic efficacy of nucleosides and nucleoside analogues as antitumor, antiviral, antiparasitic, and antiarrhythmic agents has been well documented. Pharmacokinetic studies suggest that many of these compounds are actively transported in the kidney. The goal of this study was to determine if therapeutically relevant nucleosides or analogues interact with the recently characterized Na⁺-driven nucleoside transport system of the brush border membrane of the human kidney. Brush border membrane vesicles (BBMV) were prepared from human kidney by divalent cation precipitation and differential centrifugation. The initial Na⁺-driven ³H-uridine uptake into vesicles was determined by rapid filtration. The effect of several naturally occurring nucleosides (cytidine, thymidine, adenosine), a pyrimidine base (uracil), a nucleotide (UMP), and several synthetic nucleoside analogues [zidovudine (AZT), cytarabine (Ara-C), and dideoxycytidine (ddC)] on Na⁺–uridine transport was determined. At a concentration of 100 µM the naturally occurring nucleosides, uracil, and UMP significantly inhibited Na+-uridine transport, whereas the three synthetic nucleoside analogues did not. Adenosine competitively inhibited Na+-uridine uptake with a K _i of 26.4 µM (determined by constructing a Dixon plot). These data suggest that naturally occurring nucleosides are substrates of the Na⁺–nucleoside transport system in the renal brush border membrane, whereas synthetic nucleoside analogues with modifications on the ribose ring are not. The K _i of adenosine is higher than clinically observed concentrations and suggests that the system may play a physiologic role in the disposition of this nucleoside.