紫外分光光度法测定盐酸丁卡因滴眼液的含量

目的建立盐酸丁卡因滴眼液中盐酸丁卡因含量的测定方法.方法采用紫外分光光度法测定盐酸丁卡因的含量.结果盐酸丁卡因浓度在2～12 μg/ml范围内线性关系良好(r＝0.9995),其平均回收率为99.5%,RSD为0.59%(n＝5).结论该法简便、快速,结果准确,可用于盐酸丁卡因滴眼液的质量控制.     

紫外分光光度法测定复方盐酸丁卡因含漱液中盐酸丁卡因的含量

的建立测定复方盐酸丁卡因含漱液中盐酸丁卡因含量的紫外分光光度法。方法利用盐酸丁卡因最大吸收波长，以pH值为5.8的磷酸盐缓冲液为溶剂，在310 nm波长处以紫外分光光度法测定复方盐酸丁卡因含漱液中盐酸丁卡因的含量。结果盐酸丁卡因浓度在1.26～8.82 μg·mL^-1范围内时，与吸光度呈良好的线性关系（r＝1.000 0），在测定波长处空白溶液对盐酸丁卡因测定无干扰，样品溶液在18 h内稳定，平均回收率为100.1%，RSD为0.15%（n＝9）。结论该法简便、快速、准确、重复性好，可作为复方盐酸丁卡因含漱液中盐酸丁卡因的含量测定方法。     

紫外分光光度法测定盐酸丁卡因含量

目的建立紫外分光光度法测定复方盐酸丁卡因含漱液中的盐酸丁卡因含量,有效控制药品质量。方法利用盐酸丁卡因最大吸收波长,在311nm处紫外分光光度法测定含量。结果盐酸丁卡因含量测定方法的线性范围为1～9μg·mL-1,其回归方程为y=0.076x 0.0045(n=5,r=1.0000),平均回收率为101.3%,RSD为0.78%(n=9)。在测定波长处空白溶液对盐酸丁卡因测定无干扰,样品溶液在7h内稳定。结论本法快速,简便,重现性好,可用于复方盐酸丁卡因含漱液的质量控制。     

双波长法测定尿道润滑冻胶Ⅰ号盐酸丁卡因含量

目的建立测定尿道润滑冻胶I号盐酸丁卡因含量的方法。方法采用双波长分光光度法,以0.1mol.L-1盐酸为稀释液,检测波长为229和252 nm。结果盐酸丁卡因在5.0~12.0μg.mL-1浓度范围内有良好的线性关系,r=0.999 91;平均回收率为100.13%,RSD为1.14%。结论该法简便,定量准确,可作为尿道润滑冻胶I号盐酸丁卡因含量测定方法。     

紫外分光光度法测定盐酸丁卡因胶浆的含量

目的：建立盐酸丁卡因胶浆的含量测定方法。方法：采用紫外分光光度法在310nm波长处测定盐酸丁卡因胶浆的含量。结果：平均回收率为100．38％，RSD为1．22％，与永停滴定法进行对比，无显著性差异。结论：该法具有方法简便迅速、灵敏度高的特点，可用于盐酸丁卡因胶浆中间体的含量测定。     

紫外分光光度法测定电光性眼炎滴眼液中的丁卡因

目的研究电光性眼炎滴眼剂中盐酸丁卡因的含量测定方法,以解决中和法测定盐酸丁卡因的含量受盐酸肾上腺素影响的问题。方法以蒸馏水为溶媒,用分光光度法进行测定。结果盐酸丁卡因在2~20μg·ml-1之间线性关系良好(r=0.9999),回收率为100.4%,RSD=0.82%(n=6)。结论所用方法简便、准确、重复性好,解决了原中和法无法准确测定电光性眼炎滴眼剂成品中盐酸丁卡因含量的问题。     

盐酸丁卡因含量和有关物质检测研究进展

目的:为盐酸丁卡因原料药及制剂的质量控制提供参考。方法:以"盐酸丁卡因"、"有关物质"和"测定"等为关键词对相关数据库进行检索,对其中收录的盐酸丁卡因原料药及制剂的含量和有关物质测定方法相关文献作简要综述。结果与结论:盐酸丁卡因原料药和含量较高的制剂可采用电位滴定法测定其含量;盐酸丁卡因含量较低且基质简单的制剂常用紫外-可见分光光度法测定其含量;而高效液相色谱法则适用于含量较低且基质较为复杂的盐酸丁卡因制剂的含量测定。盐酸丁卡因原料药及制剂中有关物质的测定以高效液相色谱法更为适用。     

HPLC法测定复方地塞米松丁卡因乳膏中醋酸地塞米松和盐酸丁卡因的含量

建立复方地塞米松丁卡因乳膏中醋酸地塞米松、盐酸丁卡因含量的HPLC测定方法。色谱柱为SUNTEK Kromasil C18;流动相为甲醇-水-三乙胺(75∶25∶0.04),流速为1.0mL.min-1,检测波长为240 nm,线性范围:醋酸地塞米松2.5~20μg.mL-1,盐酸丁卡因100~800μg.mL-1,r=0.9999。平均回收率:醋酸地塞米松为100.12%,RSD为0.89%;盐酸丁卡因为98.63%,RSD为0.97%。方法准确可靠,简单易行,可用于复方地塞米松丁卡因乳膏中醋酸地塞米松、盐酸丁卡因的含量测定。     

微柱离心-HPLC法测定盐酸丁卡因脂质体包封率

目的:建立测定盐酸丁卡因脂质体包封率的方法。方法:采用微柱离心法分离脂质体与游离药物,以高效液相色谱法测定药物浓度并计算包封率。结果:微柱离心法能很好地将脂质体与游离药物分离,空白脂质体的回收率为90.4%～100.1%,游离药物吸附率为96.6%～99.2%;盐酸丁卡因脂质体包封率均在80%左右。结论:所建盐酸丁卡因脂质体包封率的测定方法简单、快速、重现性好。     

紫外法与亚硝酸钠法测定盐酸丁卡因含量

10%盐酸丁卡因注射液是临床常用的麻醉剂,其制备方法与检查均按《黑龙江省医院制剂规范》执行,其含量测定方法为亚硝酸钠法。由于盐酸丁卡因在紫外区有吸收,根据这一特点,用紫外分光光度法测定盐酸丁卡因注射液含量与亚硝酸钠法做对照实验,结果满意,两种方法无显著性差异(P>0.1),回     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

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Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

Aquatic Insects and Trace Metals: Bioavailability,Bioaccumulation, and Toxicity

Abstract

The uptake of metals from food and water sources by insects is thought to be additive. For a given metal, the proportions taken up from water and food will depend both on the bioavailable concentration of the metal associated with each source and the mechanism and rate by which the metal enters the insect. Attempts to correlate insect trace metal concentrations with the trophic level of insects should be made with a knowledge of the feeding relationships of the individual taxa concerned. Pathways for the uptake of essential metals, such as copper and zinc, exist at the cellular level, and other nonessential metals, such as cadmium, also appear to enter via these routes. Within cells, trace metals can be bound to proteins or stored in granules. The internal distribution of metals among body tissues is very heterogeneous, and distribution patterns tend to be both metal and taxon specific. Trace metals associated with insects can be both bound on the surface of their chitinous exoskeleton and incorporated into body tissues. The quantities of trace meals accumulated by an individual reflect the net balance between the rate of metal influx from both dissolved and particulate sources and the rate of metal efflux from the organism. The toxicity of metals has been demonstrated at all levels of biological organization: cell, tissue, individual, population, and community. Much of the literature pertaining to the toxic effects of metals on aquatic insects is based on laboratory observations and, as such, it is difficult to extrapolate the data to insects in nature. The few experimental studies in nature suggest that trace metal contaminants can affect both the distribution and the abundance of aquatic insects. Insects have a largely unexploited potential as biomonitors of metal contamination in nature. A better understanding of the physico-chemical and biological mechanisms mediating trace metal bioavailability and exchange will facilitate the development of general predictive models relating trace metal concentrations in insects to those in their environment. Such models will facilitate the use of insects as contaminant biomonitors.     

Alzheimer’s disease – current trends in basic and clinical research. Highlights from the 16th ECNP

Advances in the molecular biological knowledge of neuronal nicotinic acetylcholine receptors (nAChRs) have led to a growing interest by the pharmaceutical industry in the development of novel compounds that selectively modulate nAChR function. The ability of (-)-nicotine, an activator of nAChRs, to enhance attentional aspects of cognition in animals and humans, to exert neuroprotective and anxiolytic-like effects, and presumably to mediate the negative correlation between smoking and Alzheimer's (and Parkinson's) Disease, has focused interest on the potential therapeutic utility of modulators of nAChR function for treatment of some of the deficits associated with these progressive, neurodegenerative conditions. Numerous compounds are known which activate nAChRs and which might serve as lead compounds toward the development of such agents. The pharmacologic diversity of neuronal nAChR subtypes suggests the possibility of developing selective compounds which would have more favourable side-effect profiles than existing agents. This broader class of agents, collectively called cholinergic channel modulators (ChCMs), is anticipated to encompass compounds which would have more favourable side-effect profiles than existing agents, which generally exhibit low selectivity. This selectivity may be achieved by preferentially activating some subtypes of nAChRs (i.e., Cholinergic Channel Activators, ChCAs) or inhibiting the function of other subtypes (Cholinergic Channel Inhibitors, ChCIs). An overview of the biology of nAChRs and the rationale for the use of ChCMs for the treatment of dementia related to neurodegenerative diseases are presented, followed by a discussion of lead compounds and compounds under consideration for clinical evaluation.     

2-(Acetoxyphenyl)-(Z)-styryl sulfides as cyclooxygenase inhibitors

2-(Acetoxyphenyl)-(Z)-styryl sulfides are described as selective cyclooxygenase-2 (COX-2) inhibitors, useful for treating inflammation and COX-2-mediated disorders including neoplasia. 2-(Acetoxyphenyl)-(Z)-styryl sulfide is claimed to be the most potent COX inhibitor in the series with a COX-2 selectivity ratio of 33. This compound is also claimed to be superior to celecoxib (Celebrex^®, Pfizer) in inhibiting cell growth of colorectal carcinoma cells. In this evaluation, the COX inhibitory activity of this compound is compared to that previously disclosed for diarylheterocycles and 2-(acetoxyphenyl)alkyl sulfides. The validity of the DLD-1 cell line in the growth inhibition studies is questioned based on recent literature reports indicating the lack of COX-2 expression in this cell line.     

Sleep-disordered breathing with chronic opioid use

Chronic opioid use for pain relief or as substitution therapy for illicit drug abuse is prevalent in our societies. In the US, retail distribution of methadone and oxycodone has increased by 824 and 660%, respectively, between 1997 and 2003. μ-Opioids depress respiration and deaths related to illicit and non illicit chronic opioid use are not uncommon. Since 2001 there has been an emerging literature that suggests that chronic opioid use is related to central sleep apnoea of both periodic and non-periodic breathing types, and occurs in ～ 30% of these subjects. The clinical significance of these sleep-related abnormalities are unknown. This review addresses the present knowledge of control of ventilation mechanisms during wakefulness and sleep, the effects of opioids on ventilatory control mechanisms, the sleep-disordered breathing found with chronic opioid use and a discussion regarding the future research directions in this area.     

Drug targets for cognitive enhancement in neuropsychiatric disorders

The investigation of novel drug targets for treating cognitive impairments associated with neurological and psychiatric disorders remains a primary focus of study in central nervous system (CNS) research. Many promising new therapies are progressing through preclinical and clinical development, and offer the potential of improved treatment options for neurodegenerative diseases such as Alzheimer's disease (AD) as well as other disorders that have not been particularly well treated to date like the cognitive impairments associated with schizophrenia (CIAS). Among targets under investigation, cholinergic receptors have received much attention with several nicotinic agonists (α7 and α4β2) actively in clinical trials for the treatment of AD, CIAS and attention deficit hyperactivity disorder (ADHD). Both glutamatergic and serotonergic (5-HT) agonists and antagonists have profound effects on neurotransmission and improve cognitive function in preclinical experiments with animals; some of these compounds are now in proof-of-concept studies in humans. Several histamine H3 receptor antagonists are in clinical development not only for cognitive enhancement, but also for the treatment of narcolepsy and cognitive deficits due to sleep deprivation because of their expression in brain sleep centers. Compounds that dampen inhibitory tone (e.g., GABA_A α5 inverse agonists) or elevate excitatory tone (e.g., glycine transporter inhibitors) offer novel approaches for treating diseases such as schizophrenia, AD and Down syndrome. In addition to cell surface receptors, intracellular drug targets such as the phosphodiesterases (PDEs) are known to impact signaling pathways that affect long-term memory formation and working memory. Overall, there is a genuine need to treat cognitive deficits associated with many neuropsychiatric conditions as well as an increasingly aging population.