Anti-social personality disorder and response to methadone maintenance treatment

A sample of 183 current methadone maintenance patients were interviewed on their drug use history, criminal history, current drug use, and symptoms of Anti-social Personality Disorder (ASPD). Thirty-nine percent of patients met the DSM-III-R criteria for a diagnosis of ASPD. ASPD patients had an earlier onset of drug use, drug injecting, heroin use, had wider polydrug using histories and had been arrested earlier and more frequently than other patients. Despite the different pretreatment histories of ASPD and other patients, there were no differences between the two groups in retention in treatment, methadone dosage or heroin use. It is concluded that heroin-dependent ASPD patients can be successfully retained in methadone treatment, on similar methadone doses and with similar in-treatment drug use patterns as those of non-ASPD heroin dependent patients.     

The case for liver transplantation in end-stage alcoholic liver disease

Liver transplantation is now a routine procedure and is seen as a valid treatment option for end-stage liver disease. Alcoholism has been regarded as a relative or absolute contraindication to liver transplantation in many transplant units. Recent data document a success rate for transplantation in alcoholic patients that equals that in other patient groups. Issues relating to the ethical and scientific arguments surrounding this complex area of treatment are discussed. It is concluded that individual patients should be assessed in their own right for this treatment option. It is argued that patient groups should not be denied access to specific life-saving treatments.     

Potassium-selective channels in the basolateral membrane of single proximal tubule cells of frog kidney

The membrane potential of proximal tubule cells is dominated by the potassium conductance of the basolateral membrane. In the present paper the nature of this conductance is investigated by the patch-clamp technique. Only one type of K channel was found in the basolateral membranes of freshly isolated proximal cells. In cell-attached patches, the current/voltage relationship is markedly non-linear with much larger inward (30 pS) than outward ( 6 pS) conductances, even in the presence of roughly symmetrical K concentrations. Thus the channels show inward rectification. The determination of the conductance for outward current flow is complicated since the current/voltage curves show an area of negative conductance. Nevertheless, taking the conductance for outward current flow and the density of the channels it is possible to account for all of the previously reported potassium conductance of amphibian proximal tubule cells. The open probability of the channels was found not to depend upon the membrane potential. However, the non-linearity of the current/voltage relationships will confer upon the channel the same voltage dependence as that seen in intact proximal tubules, i.e. the conductance decreases with depolarisation. Incubation of cells in Ringer with no substrates or in the presence of alanine and/or glucose showed no change in the activity of the channels. These findings suggest that, although these channels may represent the basolateral conductance of frog proximal tubule cells, they are not involved in the well-established coupling between transport rate and potassium conductance.This work was supported by the Wellcome Trust     

Evidence of a preferential role of brain serotonin in the mechanisms leading to naloxone-precipitated compulsive jumping in morphine-dependent rats

Various drugs acting on brain serotonin or catecholamines were administered concurrently with morphine during the development of dependence or before naloxoneprecipitated withdrawal syndrome. Of the various drugs only cyproheptadine, a serotonin antagonist, and piribedil, a dopamine agonist, reduced the frequency of jumping (but not of diarrhea or ptosis) when administered with morphine during development of dependence. When administered before naloxone, d-fenfluramine, a serotonin releaser, markedly reduced jumping, but not diarrhea and ptosis, and clonidine blocked these latter signs without affecting the frequency of jumping. Of the other drugs examined only phenoxybenzamine reduced diarrhea in morphine-abstinent rats. It is suggested that serotonin is involved in the mechanisms which lead to compulsive jumping during naloxoneprecipitated withdrawal, whereas adrenergic sites on which clonidine acts are mainly involved in the expression of signs, such as ptosis and diarrhea. No clear evidence was obtained of a role for dopamine in the withdrawal signs studied.     

Précipitation et prévention de l'abstinence chez le rat et la souris en état de dépendance aiguë. Comparaison de la naloxone,de la naltrexone et de la diprenorphine

Summary Abstinence signs were precipitated in rats by naloxone (1 mg·kg^-1 s.c.) injected at various times (from 1.5 to 16 h) after a single dose of morphine hydrochloride (15 or 50 mg·kg^-1 s.c.) administered incaqueous solution. Increasing the dose of morphine increased the latency of the phenomena and the duration of the underlying state shifts of signs as described by Bläsig et al. (1974) in chronically morphinized rats also occurred when increasing the dose of morphine and the time interval between the injections of morphine and of naloxone. Naltrexone and diprenorphine were also effective. These three antagonists, given before morphine, were able to prevent precipitated abstinence: however, naloxone was almost ineffective when the higher dose of morphine was used and when the time interval was long. In these latter conditions, naltrexone was definitely more effective and longer acting and diprenorphine still more so. The same characteristics were found for the protective action of the three antagonists in acutely morphinized mice and the same order for their potencies in precipitating abstinence in acutely morphinized mice. Like naloxone, naltrexone and diprenorphine facilitated a nociceptive reaction in normal mice.The abstinence signs precipitated in acutely morphinized rats or mice are probably not unmasked excitatory effects of morphine as such effects should have been increased rather than inhibited by previous administration of specific antagonists; they might correspond to potentiated effects of the antagonists themselves. The prevention by specific antagonists of the abstinence syndrome is most simply interpreted by antagonism (direct or indirect) of dependence induction, but other interpretations are not excluded.

     

Mapping of c-fos gene expression in the brain during morphine dependence and precipitated withdrawal, and phenotypic identification of the striatal neurons involved

The c-fos gene is expressed in the central nervous system in response to various neuronal stimuli. Using in situ hybridization, we examined the effects of chronic morphine treatment and withdrawal on c-fos mRNA in the rat brain, and particularly within identified striatal neurons. Morphine dependence was induced by subcutaneous implantation of two pellets of morphine for 6 days and withdrawal was precipitated by administration of naltrexone. Placebo animals and morphine-dependent rats showed a very weak c-fos mRNA expression in all the structures studied. Our study emphasized the spatial variations in c-fos mRNA expression, and also revealed a peak expression of c-fos mRNA at 1 h after naltrexone-precipitated withdrawal in the projection areas of dopaminergic neurons, noradrenergic neurons and in several regions expressing opiate receptors. Interestingly, morphine withdrawal induces c-fos mRNA expression in the two efferent populations of the striatum (i.e. striatonigral and striatopallidal neurons) both in the caudate putamen and nucleus accumbens. Moreover, the proportions of activated neurons during morphine withdrawal are different in the caudate putamen (mostly in striatopallidal neurons) and in the shell and core parts of the nucleus accumbens (mostly in striatonigral neurons). The activation of striatopallidal neurons suggests a predominant dopaminergic regulation on c-fos gene expression in the striatum during withdrawal. On the contrary, c-fos induction in striatonigral neurons during withdrawal seems to involve a more complex regulation like opioid-dopamine interactions via the mu opioid receptor and the D1 dopamine receptor coexpressed on this neuronal population or the implication of other neurotransmitter systems.     

SARS心理特征及心理干预对策与中医治疗探讨

通过临床观察传染性非典型肺炎引发的心理问题，包括恐惧非典综合征36例、一线医务人员26例及非典患者22例，系统地归纳了不同的心理特点及表现形式，并以国际流行的心理治疗法——认知行为疗法为基础，提出具体心理干预策略及中医辨证方法。通过进行心理支持及多种灵活的心理治疗干预，以及中医个体化辨证施治，促使患者摆脱了心理危机，很快得到康复。     

N-硝基-L-精氨酸抗阿片类精神依赖作用

 目的研究N-硝基-L-精氨酸(NO₂Arg)在吗啡、二氢埃托啡精神依赖形成中的作用。方法采用小鼠腹腔注射吗啡、二氢埃托啡的方法建立小鼠精神依赖的条件性位置偏爱模型；采用荧光内过滤法测定小鼠脑内NO的含量；小鼠脑内cAMP/cGMP含量采用放射免疫法测定。结果小鼠吗啡、二氢埃托啡精神依赖形成过程中脑内NO，cAMP，cGMP的含量显著上升；腹腔注射NO₂Arg5mg·kg^-1可抑制吗啡、二氢埃托啡精神依赖升高小鼠脑内NO，cAMP，cGMP含量的作用。结论NO在易化阿片类药物精神依赖形成中可能有一定作用；NO₂Arg 抑制吗啡、二氢埃托啡精神依赖形成的作用可能是通过减少小鼠脑内NO合成和调节cGMP/cAMP水平介导的。     

吗啡依赖大鼠血清尿酸及ALT、AST的检测分析

目的：检测吗啡依赖大鼠血清肝功能生化指标及核苷酸代谢参数的变化.方法：Wistar大鼠35只,随机分成5组,每组7只.第1组为对照组,给予0.9%氯化钠注射液；第2组给予盐酸吗啡20～95 mg&;#8226;kg 1&;#8226;d 1,分2次,ip,共7 d；第3组在给予盐酸吗啡的同时,给予嘌呤碱基混悬液100 mg&;#8226;kg 1&;#8226;d 1,ig,第8天给予盐酸纳洛酮4 mg&;#8226;kg 1,ip,观察戒断体征；第4组用嘌呤核苷混悬液替代嘌呤碱基混悬液,其余同第3组；第5组给予盐酸吗啡和盐酸纳洛酮,用量和用法同第3组.采用Beckman丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)及尿酸检测试剂盒测定相应指标.结果：发现了吗啡依赖大鼠血清尿酸水平升高,ALT及 AST酶活性升高.结论：吗啡可引起组织细胞嘌呤核苷酸分解代谢增强,引起肝脏功能的损伤.