QT离散度与急性心肌梗死合并室性心律失常及近期预后关系的探讨

目的　为探讨 QT离散度 (QTd)的临床意义 ,进一步评价其对急性心肌梗死 (AMI)合并室性心律失常 (VA)的诊断价值。方法　观察了 132例急性心肌梗死 (AMI组 )及 45名正常人 (对照组 )的最长 QT间期(QTm ax)、校正 QTmax(QTcmax)、最小 QT间期 (QTmin)、校正 QTm in(QTcmin)、QT离散度 (QTd)及心率校正 QTd(QTcd)的变化。结果　 1AMI组 ,QTmax、QTcmax、QTd及 QTcd均显著高于对照组 ,P<0 .0 1。2 AMI合并室性心律失常组 (VA组 ) ,QTmax、QTcm ax、QTd及 QTcd均显著高于无室性心律失常组 (NVA组 ) ,P<0 .0 1。3AMI患者 QTcd≥ 6 0 ms者 ,其 VA发生率显著高于 QTcd<6 0 ms者 ,P<0 .0 1。4AMI死亡组 QTmax、QTcm ax、QTd均显著高于存活组 ,P<0 .0 1,死亡组 QTcd高于存活组 ,P<0 .0 5。5 AMI患者 QTcd≥ 80 ms者其室颤 (VF)发生率显著高于 QTcd<80 ms者 ,P<0 .0 1。结论　 QTd或 QTcd可作为判断 AMI发生室性心律失常及近期预后的临床参考指标。     

扩张性心肌病QT离散度与室性心律失常及猝死的关系

目的 :探讨扩张性心肌病 (DCM)QT离散度 (QTd)、校正过的QT离散度 (QTcd)与室性心律失常及猝死的关系。方法 :对 10 7例DCM患者体表心电图QT间期测量值及 89例健康体检者测量值进行对比分析 ,并分析其与室性心律失常及猝死发生率间的关系。结果 :DCM组的QTd、QTcd明显高于正常对照组 (P <0 0 1) ,QTd≥ 6 0ms者室性心律失常发生率高于QTd <6 0ms者 (P <0 0 1) ,猝死者QTd、QTcd明显高于正常对照组 (P <0 0 1)。结论 :QTd可能是DCM室性心律失常及猝死监测的重要指标。     

索他洛尔对室性心律失常患者QT离散度的影响

目的观察心律失常患者QT离散度（QTd）变化及索他洛尔对其影响。方法40例30~68岁的室性心律失常患者接受索他洛尔治疗,剂量从80mg/d开始,观察2周,若疗效未达标准者,增加到120mg/d,以后根据病情变化逐渐减量。结果40例室性心律失常患者应用索他洛尔治疗有效,并发现该药在应用后延长Q-Tc（QT间期）同时,减小QT离散度,未见严重毒副作用。结论索他洛尔治疗室性心律失常,安全有效,能影响患者QT离散度,减少室性心律失常的复发及室颤发生。     

小剂量索他洛尔和美托洛尔治疗肥厚型心肌病伴恶性室性心律失常的疗效观察

目的观察小剂量索他洛尔和美托洛尔(倍他乐克)联合治疗肥厚型心肌病伴恶性室性心律失常的疗效。方法对36例肥厚型心肌病伴恶性心律失常的患者,给予索他洛尔和美托洛尔口服治疗,并对心率、QT间期最大值、QT间期最小值和QT间期离散度进行治疗前后的测量。结果治疗后,总有效率为75%,心率由基础的(84.5±5.4)次/min降至(66.5±8.3)次/min(P<0.01),QT间期最大值由治疗前的(411±34)ms延长到治疗后的(415±41)ms(P>0.05),QT间期最小值由治疗前(313±32)ms延长至(353±42)ms(P<0.01),QT间期离散度由治疗前(95±31)ms缩小至(63±20)ms(P<0.01)。无心功能恶化,不良反应轻微。结论本方法疗效确切、方便、安全,无明显致心律失常作用,值得临床推广应用。     

QT离散度与室性心律失常的相关性分析

目的 探讨QT离散度(QTd)与室性心律失常的相关性。方法 分析344例常规12导联心电图QTd值,再以其24小时动态心电监测结果,分成室性心律失常组144例,无室性心律失常组200例,测量并计算各组QTd值及心率校正后的QT离散度(QTcd)值后,进行比较。结果 室性心律失常组QTd为54±18ms,QTcd为56±19ms,无室性心律失常组QTd值为41±13ms,QTcd为41±12ms,以上4组数据相比较均有显著差异(P<0.01)。结论 QT离散度的增加与室性心律失常相关,且室性心律失常越严重,QT离散度也随之增大。     

急性心肌梗死患者室性心律失常与Q—T离散度的关系

目的探讨急性心肌梗死（AMI）患者QT间期离散度（QTd）与室性心律失常的关系。方法测量180例AMI患者心电图的QTd,对有室性心律失常组与无室性心律失常组进行比较,分析其与室性心律失常的关系。结果AMI伴室性心律失常组QTd为（88．64±25．46）ms,较无室性心律失常组的（58．28±11．46）ms明显延长（P〈0．01）。结论AMI患者发生室性心律失常与QTd增大有关,Q-Td可作为预测急性心肌梗死发生室性心律失常的一项敏感指标。     

胺碘酮对室性心律失常QTc离散度的影响

体表心电图各导联间QT间期的差异反映了心室肌复极不一致性和电不稳定性区域性变化程序,这种差异命名为QT间期离散度(QT interval dispersion,QTd),多年研究显示QTd增加可作为增加估测先天性QT间期延长综合征、充血性心力衰竭、心肌梗死并发室性心律失常时敏感的无创性方法。近年来我们观察胺碘酮对室性心律失常QTcd的影响,并与索他洛尔进行比较。现报告如下:1 资料与方法1.1 对象 本院心内科住院或门诊患者52例。均经心电图(ECG)和Holter确诊,主要是警报性室性心律失常[连发室性早搏(室早)、频发多源室早、RonT现     

美托洛尔对急性心梗QT间期离散度的影响

观察美托洛尔(Metoprolol)治疗急性心硬(AMI)伴持续性室速、室颤患者对QT间期复极离散度(QTd)的影响。16例AMI患者(男性11例,女性5例,年龄55±11a)采用美托洛尔50mg,po,qid×4wk。QT间期从395.0±8.1ms延长至436.8±11.6ms(p<0.01),总有效率100％。QTd从110.1±7.8ms降至80.8±9.0ms(p<0.05),总有效率87.5％。美托洛尔对QTd及QT间期的有效影响可减少AMI发生恶性心律失常。     

老年高血压病QT间期离散度及贝那普利的影响

目的探讨老年高血压患者QT离散度 (OTd)变化以及相关因素和贝那普利的影响。方法测定 6 7例老年高血压患者和 2 0例健康老人的QTd。 6 7例随机分为 35例贝那普利治疗组和未用贝那普利的 32例对照组。结果老年高血压患者的QTd明显大于健康对照组 (5 6± 9.2msvs 37.5±10 .6ms,P <0 0 1) ;高血压伴左室肥厚者的QTd大于无左室肥厚者 (6 8 4± 15msvs 42 .3± 10 2ms ,P <0 0 1) ;高血压伴室性心律心常者QTd明显高于无心律失常者 (6 4 3± 7.5msvs 44 .6± 6 9ms,P <0 0 1) ;贝那普利治疗前后QTd显著缩小 (5 4± 9.8msvs 34 .6± 8 8ms,P <0 0 1)。结论老年高血压患者QTd增大与高血压伴左室肥厚及室性心律失常有关 ,贝那普利治疗使QTd明显缩短。     

QTd预测缺血性室性心律失常的临床价值及其与QT间期相关性研究

目的 通过研究128例缺血性心脏病患的QTd的差异,以探讨QTd对判断室性心律失常价值。方法 根据有无室性心律失常,将患平均分成两组,室性心律失常组64例,对照组64例。使用12导联的体表心电图检查。人工分规测量QT间期和QTd。结果 有室早的QTd显高于对照组,两组有显差异(P<0.01）且QTd与QT间期无相关关系（r=0.15)。结论 QTd是预测缺血性心脏病室性心律失常简单而有效的指标。     

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.

     

In vitro studies on sterically stabilized liposomes (SL) as enzyme carriers in organophosphorus (OP) antagonism

This study describes a new approach for organophosphorous (OP) antidotal treatment by encapsulating an OP hydrolyzing enzyme, OPA anhydrolase (OPAA), within sterically stabilized liposomes. The recombinant OPAA enzyme was derived from Alteromonas strain JD6. It has broad substrate specificity to a wide range of OP compounds: DFP and the nerve agents, soman and sarin. Liposomes encapsulating OPAA (SL)* were made by mechanical dispersion method. Hydrolysis of DFP by (SL)* was measured by following an increase of fluoride ion concentration using a fluoride ion selective electrode. OPAA entrapped in the carrier liposomes rapidly hydrolyze DFP, with the rate of DFP hydrolysis directly proportional to the amount of (SL)* added to the solution. Liposomal carriers containing no enzyme did not hydrolyze DFP. The reaction was linear and the rate of hydrolysis was first order in the substrate. This enzyme carrier system serves as a biodegradable protective environment for the recombinant OP-metabolizing enzyme, OPAA, resulting in prolongation of enzymatic concentration in the body. These studies suggest that the protection of OP intoxication can be strikingly enhanced by adding OPAA encapsulated within (SL)* to pralidoxime and atropine.     

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.     

Steroidal sapogenin contents in some domestic plants

In order to find out the values of the steroid resources for the future use. the compositions and contents of steroidal sapogenins from 13 domestic plants have been investigated. As a result,Dioscorea nipponica, D. quinqueloba andSmilax china were found to have large amount of diosgenin. And pennogenin inTrillium kamtschaticum andParis verticillata, yuccagenin inAllium fistulosum, hecogenin inAgave americana and neochlorogenin inSolanum nigum were appeared to be major steroidal sapogenins.     

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.