黄腐酸钠对肝硬化大鼠肝缺血再灌注损伤的保护作用

目的　观察黄腐酸钠对肝硬化大鼠肝脏的缺血再灌注损伤的保护作用。方法　用四氯化碳橄榄油制作肝硬化大鼠模型后 ,术前 3d灌胃 2 %黄腐酸钠 10 0mg/ (kg·d) ,每天两次。两次肝门阻断后于下腔静脉取血 ,检测血清ET 1、TNF α、IL 6值 ,同时取肝左叶肝脏组织病理检查。结果　术后黄腐酸钠组血清ET 1、TNF α、IL 6值均较对照组降低。与对照组比较均有显著性意义 (P <0 0 5 )。光学显微镜检查 ,黄腐酸钠组的肝细胞病理损伤程度比对照组轻。结论　术前用黄腐酸钠对肝硬化大鼠的肝缺血再灌注损伤有明显的保护作用。     

脂质体制剂影响大鼠皮肤超微结构的初步研究

目的：研究脂质体制剂对大鼠皮肤超微结构的影响。方法：取健康大鼠背部皮肤，分别浸入空白脂质体混悬液、0．125％脂质体荧光素钠混悬液、PBS溶液中，8h后在H-600型透射电镜下观察皮肤超微结构的变化，以未经任何处理的同一大鼠背部皮肤作为正常对照。结果：经脂质体混悬液处理的大鼠皮肤表皮，尤其是皮肤角质层深层结构发生了明显改变，表现为角质浅层疏松，细胞问裂隙增大，电子密度增强，深层张力丝明显增多；棘层细胞胞质中板层小体增多。结论：表皮各层超微结构的改变可能与脂质体增加药物渗透性的机理有关。     

New ion exchange materials for use in a Sr/Rb generator

⁸²Rb is a short-lived positron-emitting isotope (T_1/2=75 s) that is increasingly being used in positron emission tomography for the evaluation of myocardial perfusion. The short half-life of ⁸²Rb results in rapid decay of the administered radioactivity allowing repeat scans to be performed after a relatively short time interval. The ⁸²Rb is available from a ⁸²Sr/⁸²Rb generator in which the ⁸²Sr parent is immobilized on an ion exchange column and ⁸²Rb eluted when required. Consequently, suitable ion exchangers for use in a generator must have a very high affinity for strontium and a negligible affinity for rubidium, allowing the pure ⁸²Rb to be safely and efficiently eluted in high yields. This study evaluated a number of strontium-selective ion exchange materials using batch experiments and identified sodium nonatitanate as the best material for use in a ⁸²Sr/⁸²Rb generator.     

Similar effects of cis-diamminedichloroplatinum(II) and cis-diammine-1, 1-cyclobutanedicarboxylatoplatinum(II) on sodium-coupled glucose uptake in renal brush-border membrane vesicles

cis-Diamminedichloroplatinum(II) (cDDP) has been shown to interfere with reabsorption processes in renal tubular epithelia, leading to polyuria, magnesium and sodium wasting and glucosuria. cDDP inhibits the Na⁺-coupled uptake of methyl-α-d-glucopyranoside (MGP) in renal proximal tubular cells in primary culture. cis-Diammine-1,1-cyclobutane dicarboxylatoplatinum(II) (CBDCA) produces tubular injury qualitatively similar to that of cDDP with a reduced severity. CBDCA inhibits Na⁺-coupled MGP uptake in renal proximal tubular cells in primary culture at concentrations 20- to 30-times higher than those of cDDP. The Na⁺/glucose cotransport protein possesses sulphydryl groups (SH) essential for its activity. Platinum complexes have strong affinity for SH groups. We compared the direct effects of cDDP (0.04–1.0 mM) and CBDCA (1–30 mM) on Na⁺-coupled MGP uptake in rabbit renal brush-border membrane (BBM) vesicles. cDDP and CBDCA inhibited Na⁺-coupled MGP uptake in a concentration-dependent manner, mainly through a decrease in V _max of the cotransport protein. These effects were associated with platinum binding to BBM and decreases in protein-bound SH groups. CBDCA altered Na⁺-coupled MGP uptake at concentrations 30-times higher than those of cDDP. When BBM vesicles were preincubated with cDDP or CBDCA, diethyldithiocarbamate (an antidote against cDDP-induced nephrotoxicity) partly restored Na⁺-coupled MGP uptake and reduced the amount of platinum bound to BBM, but did not restore protein-bound SH groups. These findings strongly suggest that the inhibition of Na⁺-coupled MGP uptake by cDDP and CBDCA is mainly mediated by direct chemical binding of platinum to essential SH groups of the cotransport protein but may also involve other nucleophilic groups, such as the SCH₃ group of methionine residues. Received: 22 April 1998 / Accepted: 21 July 1998     

两种不同因素对胰腺腺泡细胞损害机制的研究

目的探讨蛙皮素和牛磺胆酸钠这两种不同因素对胰腺腺泡细胞的损害机制.方法采用一步消化法分离Wistar大鼠胰腺腺泡细胞,然后与不同浓度蛙皮素、牛磺胆酸钠共同孵育,采用台盼蓝法和双标法测定细胞活率、全自动生化仪测定淀粉酶浓度、比色法测定乳酸脱氢酶浓度、激光显微共聚焦法测定钙离子波动和浓度.结果蛙皮素处理后,腺泡细胞仍保持较高的活率,淀粉酶分泌率明显上升,同时乳酸脱氢酶漏出率增加,与淀粉酶分泌率之比约为4：1;而胆酸钠处理后细胞活率明显下降,淀粉酶分泌率明显升高的同时伴有乳酸脱氢酶漏出率也等比例的增加.蛙皮素可引起胰腺腺泡细胞内游离钙离子脉冲式升高,其波动方向由分泌极向基底极;牛磺胆酸钠引起细胞内钙离子持续低幅增高,细胞两极间未出现钙离子波动.结论蛙皮素及牛磺胆酸钠通过不同机制影响胰腺腺泡细胞的存活率,导致胰腺细胞损害.     

丹奥治疗下肢闭塞性动脉硬化的疗效观察

目的:观察丹奥联合低分子肝素钙治疗下肢闭塞性动脉硬化疗效,寻找治疗该病的新途径。方法:将75例患者随机分为治疗组38例和对照组37例,两组均给以低分子肝素钙5000U每12h一次皮下注射,治疗组加用丹奥160mg加生理盐水或5%葡萄糖250mL 1次/d,静滴,对照组采用加用维脑路通400~800mg加生理盐水或5%葡萄糖250mL每日1次静滴,两组均2周为一疗程。结果:治疗组显效率、临床症状评分结果、ABI测定结果、血流变学指标均优于对照(P<0.05)。结论:丹奥配合低分子肝素钙治疗下肢闭塞性动脉硬化疗效显著,且安全无副作用,值得推广。     

低浓度利多卡因对大鼠海马CA1区缺氧神经元持续钠电流的影响

目的观察低浓度利多卡因对大鼠海马CA1区缺氧神经元持续钠电流的影响,探讨其对缺血脑损伤保护作用的机制。方法酶消化法急性分离SD大鼠海马CA1区锥体细胞,随机分为7 组(n=10):缺氧组(C组)、利多卡因1μmol·L-1组(L1组)、3μmol·L-1组(L2组)、6μmol·L-1组(L3组)、10 μmol·L-1组(L4组)、20μmol·L-1组(L5组)、30μmol·L-1组(L6组)。以全细胞膜片钳技术记录各组缺氧前持续钠电流的基础值后,C组以无糖缺氧灌流液、L1-6组以含有不同浓度利多卡因的无糖缺氧灌流液在20 s内快速置换灌流液,建立体外神经元缺氧模型。记录缺氧5 min时各组神经元的持续钠电流。结果与基础值比较,各组神经元在缺氧5 min时持续钠电流均增大(P<0.01)。在缺氧5 min 时,L1-6组持续钠电流均低于C组,L2-6组均低于L1组,L3-6组均低于L2组,L4-6组均低于L3组(P< 0.01)。结论低浓度利多卡因能抑制大鼠海马CA1区神经元缺氧引起的持续钠电流增加,该作用在10 μmol·L-1时达到最大。     

低温氧等离子体改性海藻酸钠膜分离乙醇—水溶液

研究了氧等离子体对海藻酸钠膜的表面改性，并将该膜用于渗透汽化分离乙醇－水溶液。通过红外光谱、表面电阻、接触角等手段测试，表明在海藻酸钠膜表面增加了羟基、羧基及羰基，因而更加亲水。当分别用未处理的原始膜，氧等离子体处理膜处理表面对着原料液，以及处理表面对着减压侧用于渗透汽化法分离乙醇－水混和物时，性能明显不同。其结果是：上表面处理后，渗透通量明显增加，分离系数也较未处理略高；下表面处理后，渗透速度下     

Frequency-dependent effects of amitriptyline and maprotiline on conduction in the guinea pig His-Purkinje-system in vivo

In the Cardiac Arrhythmia Suppression Trial antiarrhythmic drug therapy with slow kinetic sodium channel blockers (class Ic antiarrhythmic drugs) was associated with excess mortality, presumably due to drug induced proarrhythmia. It has been suggested that the degree of rate-dependent conduction slowing produced by agents that have sodium channel blocking properties may be related to the proarrhythmic propensity of these agents.In the present study, rate-dependent conduction slowing by the antidepressants amitriptyline and maprotiline was investigated in anesthetized guinea pigs. After electrical ablation of the sinus node the left atrium was stimulated at cycle lengths between 200 ms and 500 ms. His bundle electrograms were registered by means of an epicardial electrode. Drugs were administered by i.v. infusion of 0.2 mg kg^–1 min^–1 for 30 min followed by 0.1 mg kg^–1 min^–1 for up to 30 min. Both drugs produced substantial rate-dependent conduction slowing within the His-Purkinje-system. The relationship between pacing rate and conduction slowing was well fitted by linear regression. The steepness of the regression line was significantly greater for amitriptyline than for maprotiline (slope factors: 9.10×10^–4±7.85 × 10^–5, n = 6, vs. 6.29×10^–4±2.97×10^–5, n=6, P<0.001), indicating that conduction slowing by amitriptyline exhibits a greater degree of rate-dependence than conduction slowing by maprotiline. On abruptly changing the driving cycle length from 500 ms to 300 ms, conduction slowing reached a new steady state with rate constants of 0.83±0.093 beat^–1 (amitriptyline) and 0.14±0.05 beat^–1 (maprotiline, P<0.001). Following interruption of rapid pacing at a cycle length of 250 ms, conduction slowing recovered with time constants of 332.4±52.8 ms (amitriptyline) and 1088.1 ± 143.5 ms (maprotiline, P = 0.001). Thus, amitriptyline exhibited fast kinetic properties similar to class Ib antiarrhythmic action while the slower kinetic properties of maprotiline resembled those of class Ia agents.Deceased Correspondence to: H. Todt at the above address     

hNIS基因的组织特异性表达介导肝癌细胞摄取99Tcm

目的探讨人钠／碘同向转运体（hNIS）基因在肝癌细胞中的组织特异性表达介导^99Tc^m摄取的可行性。方法构建鼠白蛋白基因启动子／增强子（mAlb）引导下hNIS和潮酶素共同表达的逆转录病毒载体，该重组逆转录病毒感染大鼠肝癌细胞MH3924A建立稳定表达细胞系，用^125I摄取实验证实hNIS基因的功能表达。建立肝癌移植瘤大鼠模型。在体内和体外水平评价重组肝癌细胞对^99Tc^m的摄取和流出。绘制时间-放射性曲线和体内外放射性分布图。结果重组质粒构建成功。体外培养条件下，hNIS基因稳定转染细胞系摄取^99Tc^m高出野生型肝癌细胞254倍。50μmol／L NaClO3和500μmol／L哇巴因（Ouabain）可分别使MHm AlbhNIS6细胞摄取^99Tc^m降低97．56％和88．20％（P均〈0．01）。而^99Tc^m流出迅速，有效半减期不足2min，应用^99Tc^m／γ相机系统获得了转染肿瘤的清晰图像及定量数据，注射^99Tc^m O4^-后30min，MHmAlbhNIS6细胞形成的移植瘤摄取^99Tc^m比对照组高4倍。结论证实hNIS基因在肝癌细胞中的组织特异性表达介导^99Tc^m摄取；利用^99Tc^m／γ相机系统可无创、简单、定量检测hNIS基因的表达。