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1.
Mianserin markedly and selectively increases extracellular dopamine in the prefrontal cortex as compared to the nucleus accumbens of the rat 总被引:1,自引:1,他引:0
The atypical antidepressant mianserin, administered at doses of 1, 5 and 10 mg/kg SC, dose-dependently increased up to about 6 times extracellular dopamine in the medial prefrontal cortex of the rat, as estimated by vertical concentric microdialysis probes. Mianserin failed to modify extracellular dopamine in the nucleus accumbens. Mianserin also dose-dependently increased extracellular noradrenaline in the prefrontal cortex. Yohimbine, an 2 antagonist, increased extracellular dopamine in the prefrontal cortex but the maximal increase was lower than that elicited by mianserin. Yohimbine also increased extracellular noradrenaline in the prefrontal cortex, but to a lesser extent than dopamine. Clonidine, an 2 agonist, decreased extracellular dopamine and noradrenaline in the prefrontal cortex but failed to affect extracellular dopamine in the nucleus accumbens. Ritanserin, a 5HT2 antagonist, at doses of 1.0 mg/kg, failed to increase extracellular dopamine in the prefrontal cortex, but significantly potentiated the increase in extracellular noradrenaline due to yohimbine. Ritanserin failed to potentiate the increase in extracellular noradrenaline elicited by yohimbine in the prefrontal cortex. The results are interpreted to indicate that mianserin increases extracellular DA as a result of the concurrent blockade of 2 and 5HT2 receptors. Failure to affect extracellular dopamine in the nucleus accumbens is explained as due to the lack of a significant effect of 2 and 5HT2 tone on DA release in the nucleus accumbens as compared to the prefrontal cortex. The results are consistent with the postulated relationship between antidepressant drug action and the ability to increase extracellular dopamine in the prefrontal cortex. 相似文献
2.
Summary Adrenergic mechanisms were analysed in the pithed rat to determine to what extent the actions of drugs observed in vitro are relevant in situ.The drugs examined were those which are known to block the neuronal or extraneuronal uptake of noradrenaline (cocaine, desipramine and corticosterone) or to be antagonists at post and/or pre-junctional -adrenoceptors (prazosin and yohimbine) together with the antidepressant, mianserin, which has been implicated in several of these actions. These drugs were tested against the arterial diastolic pressor, cardiac chronotropic and vas deferens responses to sympathetic nerve stimulation, to indirect sympathomimetics or to direct sympathomimetics, which were chosen according to whether they were substrates for noradrenaline uptake processes or selective between adrenoceptors.Pressor and cardiac responses to sympathetic nerve stimulation or to intravenous noradrenaline were potentiated by blockade of neuronal uptake but only the pressor effect of noradrenaline was potentiated by blockade of extraneuronal uptake. The effects of the antagonists suggested that the pressor effects of noradrenaline and of sympathetic nerve stimulation result from a combination of activation of 1- and 2-adrenoceptors, but that the effect of noradrenaline had a relatively greater contribution from the 2-adrenoceptors. Mianserin was found to potentiate adrenergic responses at low doses, to produce limited antagonism at post-junctional 1-adrenoceptors in high doses but to have no detectable effect at postjunctional 2-adrenoceptors. 相似文献
3.
Charanjit S. Aulakh James L. Hill Hakan T. Yoney Dennis L. Murphy 《Psychopharmacology》1992,109(4):444-448
Administration of various doses of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) to rats produced dose-related decreases in 1-h food intake in the food-deprived paradigm. Pretreatment with spiperone (5-HT1A/5-HT2/D2 antagonist), propranolol or CGP361A (-adrenoceptor antagonists that also have binding affinities for 5-HT1A and 5-HT1B sites) and MDL-72222 (5-HT3 antagonist) did not attenuate DOI-induced suppression of food intake. In contrast, pretreatment with metergoline (5-HT1/5-HT2 antagonist) completely blocked whereas mesulergine, mianserin and ritanserin (5-HT1C/5-HT2 antagonists) partially blocked DOI's effect on food intake. On the other hand, pretreatment with MDL-72222 but not with m-chlorophenylpiperazine (m-CPP) significantly potentiated DOI-induced suppression of food intake. Furthermore, the food intake suppressant effects of various doses of DOI were found to be similar in the Fawn-Hooded (FH) rat strain as compared to the Wistar rat strain. These findings suggest that DOI-induced suppression of food intake is mediated by stimulation of both 5-HT1C and 5-HT2 receptors. 相似文献
4.
目的建立高效液相色谱法测定盐酸米安色林片含量的方法。方法采用Shiseido C8色谱柱(4.6 mm×250 mm,5μm),以0.02 mol·L-1辛烷磺酸钠溶液(用30%磷酸溶液调节p H值至3.0)-甲醇(40∶60)为流动相,流速1.0 m L·min-1,检测波长:279 nm,柱温:35℃,进样量:20μL。结果盐酸米安色林线性范围为0.026 7~0.428 mg·m L-1(r=0.999 9);平均回收率为100.21%,RSD为0.36%(n=9)。结论本法操作简便,结果准确、可靠,可作为盐酸米安色林的含量测定。 相似文献
5.
《Neurologia i neurochirurgia polska》2014,48(2):141-143
Nummular headache (NH) is a rarely recognized primary headache, the diagnostic criteria of which are contained in the appendix to the 2nd edition of the International Classification of Headache Disorders (code A13.7.1).We present the case of a 61-year-old female who suffers, regardless of NH, from right-sided occipital neuralgia. The applied treatment – gabapentin and mianserin – had no effect. Injection of bupivacaine twice to the right occipital region resulted in neuralgia resolution up to three months, with no effect on NH.This confirms the independence of two abovementioned head pain conditions. 相似文献
6.
目的:考察米安色林与SSRI治疗对男性抑郁症引起性功能障碍的差异。方法:选择2010年2月至2013年4月本院精神科门诊治疗的男性抑郁症患者95例,随机分为两个组别,45例米安色林组,50例SSRI治疗组,治疗2个疗程,收集两个组别治疗前后的HAMD和IIEF-5评分。结果:两个组别的疗效无显著差异(P〉0.05)。两个组别治疗前和治疗2w的HAMD与治疗前的IIEF-5评分无显著差异(P〉0.05)。与米安色林组比,SSRI组治疗5~10w的HAMD和治疗2—10w的IIEF-5评分有显著差异(P〈0.05)。结论:米安色林与SSRI类抗抑郁药有着同样肯定的疗效,能够改善性功能障碍。 相似文献
7.
RATIONALE: A large proportion of patients with major depression do not respond sufficiently to any first-line treatment. OBJECTIVES: The aim of this study was to compare a strategy of sertraline dose increase with a strategy of adding mianserin in patients with major depression insufficiently responding to 6 weeks of open treatment with sertraline, controlling for the effect of an extended duration of treatment. METHODS: One thousand six hundred and twenty-nine patients, 18-65 years of age, with major depression scoring at least 18 on the 17-item Hamilton depression scale (HDS) were treated openly with 50 mg/day sertraline, and patients who after 4 weeks had not responded (achieving at least a 50% reduction in score on the HDS) were treated with 100 mg/day sertraline for an additional 2-week period. The patients who had still not responded were then randomised to double-blind treatment for an additional 5 weeks with either 100 mg/day sertraline plus placebo, 200 mg/day sertraline plus placebo or 100 mg/day sertraline plus 30 mg/day mianserin. RESULTS: After 6 weeks of open treatment, 60% had responded and 22% had dropped out, leaving 295 non-responding patients (18%) for randomisation. In the intention-to-treat-analysis, continuing the treatment with 100 mg/day sertraline resulted in response in 70% of the non-responders, similar to the response rate (67%) obtained in the patients who had mianserin added. However, increasing the sertraline dose to 200 mg/day resulted in a lower response rate at 56% ( P<0.05). Similar results were seen in the completers. A substantial increase in the accumulated response rate from week 6 to week 8 was seen. There was no influence of baseline variables, including the presence of melancholic features on the overall post-randomisation response rate. CONCLUSION: After 6 weeks of insufficient antidepressant treatment with 50-100 mg/day sertraline, a continued treatment with 100 mg/day sertraline can be considered until at least week 8 before considering changing strategy, unless the condition deteriorates. 相似文献
8.
The reduction of pain by two antidepressants, clomipramine and mianserin, was, in this study on 253 patients with chronic idiopathic pain syndrome, found to be not better than a placebo when all patients were compared independently of the classification of pain. The improvement rate was around 40% after 6 weeks of treatment when using a 50% or better reduction in pain level. However, in patients who fulfilled a checklist definition of minor to major depression (30% of the total patient material) clomipramine was superior to mianserin and placebo with an improvement rate of 75% after 6 weeks. Using pain curves over time as outcome measure in the various clinical pain categories it was found that both mianserin and clomipramine seemed superior to placebo in patients with tension headache, but in patients with low back pain syndrome placebo was superior to the two antidepressants. No difference among the three treatments was found in patients with burning mouth syndrome or in patients with abdominal pain. These differences underline the importance of studying specific pain syndromes rather than composite groups of patients with idiopathic pain. The clinical significance of these pain curves needs further placebo controlled investigations. 相似文献
9.
Nobukazu Kakui Fumikazu Yokoyama Koichi Kitamura Takeshi Inoue 《Pharmacology, biochemistry, and behavior》2009,92(3):393-398
Mirtazapine is an antidepressant with a unique mechanism of action and has been categorized as a Noradrenergic and Specific Serotonergic Antidepressant (NaSSA). Although numerous clinical trials suggested the usefulness of mirtazapine for not only major depressive disorders but also a variety of anxiety disorders, efficacy studies in animal anxiety models have been rarely reported. The present study investigated a potential anxiolytic-like profile of mirtazapine in rat conditioned fear stress model. A 5-hydroxytryptamine (5-HT) 1A receptor partial agonist, buspirone (1-5 mg/kg) exhibited a significant reduction in freezing time, and its maximal effect was reversed by a selective 5-HT1A antagonist, WAY-100635 (1 mg/kg). Mirtazapine (1-10 mg/kg) also reduced the freezing time in a dose-related fashion, a substantial proportion (approx. 50%) of which was likewise antagonized by WAY-100635 (1 mg/kg). Mianserin (1-30 mg/kg), a structural analogue for mirtazapine, was ineffective. Furthermore, co-administration of α1 adrenoceptor antagonist, prazosin (0.03 mg/kg) completely reversed mirtazapine (10 mg/kg)-induced reduction of freezing time. These findings represent the first demonstration that the anxiolytic-like action of mirtazapine involves activation of 5-HT1A receptor and α1 adrenoceptor to different extents, and are compatible with one aspect of mirtazapine's pharmacological profile as NaSSA. 相似文献
10.
Borowicz KK Banach M Zarczuk R Lukasik D Luszczki JJ Czuczwar SJ 《Psychopharmacology》2007,195(2):167-174
Rationale Epilepsy often coexists with depression. Therefore, the probability of simultaneous treatment with antiepileptics and antidepressants
and the possibility of interactions between them are relatively high.
Objective The effects of acute and chronic administration of mianserin on the protective activity of valproate (VPA), carbamazepine,
phenytoin, and phenobarbital were evaluated in the maximal electroshock in mice.
Materials and methods Animals were subjected to electroconvulsions. Undesired effects were evaluated in the chimney test (motor impairment) and
passive-avoidance task (memory deficit). Brain concentrations of antiepileptic drugs were assessed by immunofluorescence.
Results When given acutely, mianserin (at doses greater than or equal to 20 mg/kg) significantly raised the electroconvulsive threshold.
The antidepressant, at the subanticonvulsant doses, enhanced the anticonvulsant action of carbamazepine, phenytoin, and VPA.
Mianserin administered chronically at 30 mg/kg significantly decreased the electroconvulsive threshold. In contrast to acute
treatment, the antidepressant at subeffective doses diminished the anticonvulsant activity of VPA and phenytoin. Mianserin
given either acutely or chronically did not affect the brain concentrations of antiepileptic drugs, so a pharmacokinetic contribution
to the observed interactions is not probable.
Acute and chronic treatment with mianserin and its combinations with antiepileptic drugs did not impair either motor coordination
or long-term memory.
Conclusion Although acute application of mianserin may potentiate the anticonvulsant action of some antiepileptics, its chronic administration
can lead to the opposite effect. Therefore, as far as the presented results can be transferred to clinical conditions, the
antidepressant therapy with mianserin should be limited or even avoided in epileptic patients. 相似文献