自血穴位注射疗法联合马来酸茚达特罗治疗老年稳定期慢性阻塞性肺疾病的临床分析

目的探讨自血穴位注射疗法联合马来酸茚达特罗治疗老年稳定期慢性阻塞性肺疾病(COPD)的临床疗效及其对患者炎性因子、免疫功能及肺功能的影响。 方法将2015年5月至2016年5月我院收治的86例老年缓解期COPD患者分为观察组与对照组。对照组给予马来酸茚达特罗治疗，观察组在对照组治疗基础上另给予自血穴位注射疗法。治疗12周后，评价2组临床疗效。治疗前及治疗12周后，分别检测2组患者肺功能指标(FEV₁、FVC与PEF)，炎性因子(IL-8、α1-AT、IL-6及TNF-α)，免疫功能指标(IgG、IgA、CD3^＋及CD4^＋)水平。治疗期间，对2组患者的不良反应进行密切观察。 结果治疗后二组患者各项检测指标均优于治疗前。治疗12周后，观察组总有效率为90.7%，明显高于对照组的72.1%(P<0.05)。治疗12周后，观察组FEV₁、FVC与PEF等肺功能指标，IgG、IgA、CD3^＋及CD4^＋等免疫功能指标水平均明显高于对照组(P<0.05)，而IL-8、α1-AT、IL-6及TNF-α含量分别为(23.23±3.87)ng/L、(3.43±0.41)g/L、(52.25±5.38)ng/L及(43.12±3.98)ng/L，改善程度均明显优于对照组(P<0.05)。治疗期间，2组患者均未出现严重不良反应。 结论自血穴位注射疗法联合马来酸茚达特罗治疗老年稳定期COPD疗效确切，可有效改善患者炎症水平，值得进行深入研究。     

马来酸罗格列酮胃漂浮型缓释片的研究

目的：根据流体动力学平衡控释原理（HBS）研制了马来酸罗列酮胃漂浮型缓释片。方法；以体外释放度和漂浮情况为筛选指标，采用单因素考察和正交试验设计相结合， 对胃漂浮缓释片的处方、制备工艺及体外释放条件进行优化筛选；采用γ闪烁照相技术对优化处方的内漂浮情况进行胃内动态观察。结果：马来酸罗格列酮胃漂浮缓释片在释放介质中迅速起漂，持漂时间超过12h,12h达最大累积释放；初步确定在胃内滞留时间达3h以上。结论：优化处方的释放过程符合Higuchi方程，释放机制为异常扩散；胃漂浮片在胃滞时间明显长于普通片。     

POSSIBLE PARTICIPATION OF NMDA AND GLYCINE RECEPTORS BUT NOT GABAA RECEPTORS IN ENFLURANE-INDUCED OPISTHOTONUS IN MICE

1. We previously reported that volatile anaesthetics produce incidences of a transient opisthotonus in mice, a sign of CNS stimulation. This study was performed to investigate mechanisms by which enflurane-induced opisthotonus (EIO) occurs. 2. The effects of pretreatment of N-methyl-d-aspartate (NMDA) antagonists dizocilpine (MK-801; DIZ) and ketamine (KET), GABA_A antagonists picrotoxin (PIC), pentylenetetrazol (PTZ) and glycine antagonist strychnine (STR) on the incidence of EIO were determined. Prior to exposure to 2.0% enflurane in air, male ddN mice were given intraperitoneal injections of 0.2 mL saline (control), 0.5–5.0 mg/kg DIZ, 20–80 mg/kg KET, 2.9 mg/kg PIC, 40.0 mg/kg PTZ and 0.75 mg/kg STR. After the injection, the behavioural state of the mice was observed for 20 min (the pre-enflurane period). During the exposure to enflurane the time for immobilization, that is, anaesthetic induction time (IT), and the incidence of EIO were measured. 3. Dizocilpine (1.0–5.0 mg/kg) and KET (80 mg/kg) significantly (P<0.01) reduced both the incidence of EIO and IT in a dose-dependent manner. During the pre-enflurane period DIZ produced incidences (5–40%) of transient seizures in a dose-dependent manner, while KET did not induce them at all. The two GABA_a antagonists had no detectable effect on the EIO. Strychnine significantly enhanced the EIO. These CNS stimulants resulted in a 3–10% incidence of transient seizure and/or opisthotonus during the pre-enflurane period, but there was no correlation between DIZ-induced seizure and EIO. 4. These results suggest that the EIO is mediated by the NMDA and the STR-sensitive glycine receptors, but not the GABA_A receptor. We speculate that DIZ acts on the NMDA-receptor and/or disrupts the balance between the inhibitory and the excitatory systems.     

Chlormethiazole, dizocilpine and haloperidol prevent the degeneration of serotonergic nerve terminals induced by administration of MDMA (‘Ecstasy’) to rats

An investigation has been made into the effect of 3,4-methylenedioxymethamphetamine (MDMA or ‘Ecstasy’) administration on the concentration of 5-hydroxytryptamine (5-HT), uptake of [³H]5-HT and [³H]paroxetine binding in rat cerebral cortex tissue. Four days after 2 injections of MDMA (20 mg/kg i.p., 6 hr apart) the concentrations of 5-HT and its metabolite 5-HIAA were reduced by 60%. The binding of [³H]paroxetine to the presynaptic 5-HT transporter was decreased and high affinity uptake of [³H]5-HT was reduced by a similar amount, indicating neurodegeneration of 5-HT terminals. Pretreatment with chlormethiazole (100 mg/kg i.p.), 10 min before each MDMA injection prevented the decrease in both [³H]parotextine binding and uptake of [³H]5-HT. The loss in 5-HT and 5-HIAA content was also attenuated. Pretreatment with dizocilpine (1 mg/kg i.p.) or haloperidol (2 mg/kg i.p.) also prevented the MDMA-induced loss of [³H]paroxetine binding and attenuated the loss of 5-HT and 5-HIAA content. All three compounds also decreased the degree of hyperthermia that follows MDMA administration, although previous studies suggest that the long term neurodegeneration is not associated with the acute hyperthermic response. These data support the findings of others that MDMA injection produces degeneration of 5-HT nerve terminals in the cortex, confirm that chlormethiazole, dizocilpine and haloperidol attenuate MDMA-induced neurotoxic loss of 5-HT and demonstrate for the first time that these compounds prevent the neurodegeneration of 5-HT nerve terminals that follows MDMA administration.     

马来酸桂哌齐特在颅脑损伤患者的治疗效果观察

目的通过随机分组对照观察探讨马来酸桂哌齐特对颅脑损伤患者的治疗效果。方法100例急性闭合性颅脑损伤患者，分为对照组和用药组，各50例病人。分析对比治疗后对照组和用药组的实验室各项检查指标：血液流变学，TCD检查结果等变化情况。并且对出院后3—6个月随访调查结果进行比较分析。结果治疗后血液流变学检查中，用药组（马来酸桂哌齐特组）各项指标均低于对照组（P〈0．05）。经颅多普勒检测结果显示：用药组的脑血流速度与对照组相比明显减慢（P〈0．05），血管痉挛得到缓解。对比两组出院后随访结果可以看出，用药组的GOS评分、KPS评分及Barthel指数预后明显好于对照组（P〈0.05）。结论初步证明急性颅脑损伤早期应用马来酸桂哌齐特可增加病变区的脑血流，改善微循环，改善颅脑损伤患者的预后。值得推广和进一步研究。     

Incisional healing in rats treated with diethyl maleate

Diethyl maleate (DEM) which binds and thus depletes tissue glutathione levels was used to aggravate the injury and to determine its effect on incisional healing. A 5 cm dorsal midline skin incision was performed on 40 albino Wistar rats in two groups and then closed by interrupted sutures. Groups received 0.9% NaCl and DEM at a dosage of 1 mg/kg/day intraperitoneally for seven days, respectively. On postoperative days 7 and 14, histopathological assessment and tensile strengths were measured. The DEM treated group had a marked inflammation with poorly defined collagen formation and the tensile strength measurements revealed a significant decrease (p <0.001) on the 7t day. On the other hand, the first group showed better collagenization and a lesser degree of inflammation. However, on the 14th day, there was no noticeable histopathological difference between the two groups; but, tensile strength values of the second group were still lower (p <0.05). In this animal model, DEM postponed the healing process and reduced the tensile strength.     

示差导数光谱法测定感冒通片中双氯灭痛和扑尔敏的含量

本文利用示差导数光谱法对感冒通片中双氯灭痛和扑尔敏进行定量测定。本法用同一样品液,在同一测定条件下完成,具有操作简便、快速、灵敏度高和重现性好等特点,双氯灭痛和扑尔敏的平均回收率分别为99.5%和97.3%,变异系数分别为0.42%和0.63%.     

毛细管区带电泳法测定复方马来酸依那普利片中两组分含量

用毛细管区带电泳法同时测定复方马来酸依那普利片中两组分含量。以咖啡因为内标，２０ｍｍｏｌ／Ｌ硼砂—２０ｍｍｏｌ／Ｌ磷酸二氢钠（４９∶５１，ｐＨ８６）为运行缓冲液，在７ｍｉｎ内完成分离。马来酸依那普利和氢氯噻嗪的线性范围分别为８０～６４０μｇ／ｍＬ（ｒ＝０９９９９）和５０～４００μｇ／ｍＬ（ｒ＝０９９９３）。平均回收率分别为１０１０％和１０１１％，ＲＳＤ分别为１０％和１７％，ｎ＝５。     

Patch clamp studies on the kinetics and selectivity of N-methyl-d-aspartate receptor antagonism by memantine (1-amino-3,5-dimethyladamantan)

Memantine (1-amino-3,5-dimethyladamantan) was tested as an antagonist of N-methyl-d-aspartate (NMDA) receptors on cultured superior collicular and hippocampal neurones using the patch clamp technique and its actions were compared to those of Mg²⁺ ions, ketamine, dextrorphan, dextromethorphan, phencyclidine and dizocilpine (MK-801). Memantine (2–33 μM) concentration-dependently antagonized responses to NMDA 100 μM with an IC₅₀ of 2.92 ± 0.05 μM. In contrast, current responses to (S)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (l-AMPA 50–100 μM) and γ-amino butyric acid (GABA 10 μM) were unaffected by Memantine 8 μM. Memantine 8 μM caused a non-parallel shift of the NMDA concentration-response curve to the right in a manner indicative of uncompetitive open channel block. The effects of memantine were similar to ketamine in that both antagonists were weakly use- and strongly voltage-dependent. In contrast, MK-801, phencyclidine and dextrorphan showed much slower kinetics that was reflected in their marked use- and weaker voltage-dependency. The antagonistic effects of memantine were not reversed by increasing concentrations of glycine (0.1–100 μM) ruling out the possibility of an interaction of memantine with the strychnine-insensitive glycine modulatory site associated with the NMDA receptor-channel complex. Memantine (1–100 μM) also selectively antagonized responses to NMDA (40 μM) in the cortical wedge preparation with IC₅₀ of 12.9 ± 1.5 μM.