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1.
Pharmacology of spinal adrenergic systems which modulate spinal nociceptive processing 总被引:30,自引:0,他引:30
T L Yaksh 《Pharmacology, biochemistry, and behavior》1985,22(5):845-858
Spinopetal pathways may be activated by a variety of brainstem manipulations including microinjections of morphine which are known to modulate spinal nociceptive processing. Based on the ability of these manipulations to release spinal noradrenalin; the ability to reverse the antinociceptive effects by intrathecal adrenergic antagonists and the fact that intrathecal injections of noradrenalin mimic the antinociceptive effect, it appears that the descending modulation may be mediated by descending noradrenergic systems. Examination of the spinal receptor systems with intrathecally administered agents indicates that spinal alpha, but not beta adrenergic receptor agonists produce a powerful analgesia as measured on a variety of reflex and operant measures in mouse, rat, cat, primate and man. On the basis of agonist and antagonist structure-activity relationships it appears that a significant effect can be produced in the absence of any detectable effect on motor function by the occupation of spinal alpha 2 receptors. Distinguishable alpha 1 receptors also appear "analgetically-coupled," but their effects are uniformly contaminated by signs of cutaneous hyperreflexia at doses required to produce analgesia. The ordering of potency with which intrathecal adrenergic antagonists reverse the effects of intrathecal noradrenalin is indistinguishable from that of the reversal by these intrathecal agents of the antinociceptive effects evoked by brainstem morphine. This suggests that the population of spinal receptors acted upon by exogenously administered adrenergic agonists and endogenously released noradrenaline have indistinguishable characteristics. 相似文献
2.
Bela Szabo Tobias Auberle Klaus Starke 《Naunyn-Schmiedeberg's archives of pharmacology》1993,348(3):249-257
Summary Inhibition of uptake, in the central nervous system leads to a decrease of sympathetic outflow to many tissues; central a2-adrenoceptors are involved in this decrease. The aim of the present study was to compare the effects of the selective uptake, inhibitor (+)-oxaprotiline on the plasma kinetics of noradrenaline and adrenaline in anaesthetized and in conscious rabbits. [3H]Noradrenaline and [3H]adrenaline were infused iv. The arterial plasma concentrations of endogenous and radiolabelled noradrenaline and adrenaline were measured, and the clearance from and spillover into the plasma of noradrenaline and adrenaline were calculated.Results obtained in conscious and anaesthetized rabbits were similar. (+)-Oxaprotiline 0.2, 0.6 and 1.8 mg kg–1 iv. dose-dependently reduced the clearance of [3H]noradrenaline from the plasma. The clearance of [3H]adrenaline was reduced less. The spillover of endogenous noradrenaline was decreased by up to 35%. In contrast, the spillover of adrenaline tended to be enhanced. Prazosin 0.1 and 1 mg kg–1 was injected iv. in a second part of each experiment. It lowered the blood pressure and caused a marked increase in noradrenaline spillover but no increase or even a decrease in adrenaline spillover.The results are compatible with the following hypothesis. The sympathetic outflow from the central nervous system is subject to a twofold a-adrenoceptor-mediated modulation: -adrenoceptor-mediated inhibition and 1-adrenoceptor-mediated excitation. In the control of the sympathetic outflow to many extra-adrenal tissues, the 2-adrenergic inhibition prevails. Uptake1 inhibitors depress sympathetic outflow to such tissues by enhancing the 2-adrenergic inhibition. In the regulation of the sympathetic outflow to the adrenal medulla, in contrast, 2-adrenergic inhibition and 1-adrenergic excitation have a similar impact. Uptake, inhibitors, hence, cause little change in adrenaline release: the two opposing influences cancel out. Prazosin produces an increase in noradrenaline but not adrenaline release because the loss of the central 1 sympathoexcitation attenuates at best slightly the baroreflex to most extra-adrenal tissues but dampens markedly the baroreflex to the adrenal medulla.
Correspondence to B. Szabo at the above address 相似文献
3.
Certain drugs, particularly clozapine and clonidine, have been reported to increase selectively the latency to initiate brain stimulation (the ON latency) in a shuttlebox test of self-stimulation, suggesting a preferential attenuation of the "reward" component. The pharmacological selectivity of this reported effect was systematically evaluated. At doses that blocked bar-pressing self-stimulation, metoclopramide (3 mg/kg), prazosin (3 mg/kg) clonidine (0.1mg/kg), clozapine (3 mg/kg)and haloperidol (0.3 mg/kg), all elevated the ON latency to a greater extent than the OFF latency. Methocarbamol (200 mg/kg), and a muscle relaxant, also elevated the ON latency preferentially but the magnitude of this preferential effect was smaller than that produced by the other drugs. A hurdle in the center of the shuttlebox increased the ON and OFF latencies nonselectively. The shuttlebox procedure does not clearly discriminate among various substances that interfere with noradrenergic or dopaminergic neurotransmission, but the common profile produced by the these substances is distinguishable to some degree from simple motor disruption. 相似文献
4.
The mechanism of clonidine-induced hyperphagia and weight gain in monkeys was studied in 11 Stumptail macaques. Clonidine induced a significant increase in food intake over baseline levels and a significant weight gain after the 3-day treatment period. Both changes induced by clonidine were antagonized by the 2-noradrenergic antagonist yohimbine, but not by prazosin, an 2-noradrenergic antagonist. These results suggest that clonidine-induced hyperphagia and weight gain in monkeys are mediated through 2-noradrenergic receptors. 相似文献
5.
目的 以HPLC法测定盐酸哌唑嗪片的含量及有关物质。方法 采用Zorbax SB-C18色谱柱(250mm×4.6mm ,5μm) ,流动相为甲醇-水-冰醋酸-三乙胺(490∶460∶45∶5) ,流速为1.0ml·min-1,柱温30℃,检测波长为247nm ,用外标法测定。结果 盐酸哌唑嗪的保留时间约为4.2min ,且与其它峰的分离度大于1.5。盐酸哌唑嗪的线性范围为5~50μg·ml-1(r=0.9999) ,最低检测限为0.4ng·ml-1,平均回收率和RSD分别为100.8%和0.68%。结论 该方法简便、快速,结果准确可靠,适用于盐酸哌唑嗪片的含量及有关物质的定量检测。 相似文献
6.
目的 以HPLC法测定盐酸哌唑嗪片的含量及有关物质。方法 采用ZorbaxSB C1 8色谱柱(2 5 0mm×4 .6mm ,5μm) ,流动相为甲醇-水-冰醋酸-三乙胺(490∶4 6 0∶4 5∶5 ) ,流速为1 . 0ml·min-1 ,柱温30℃,检测波长为2 4 7nm ,用外标法测定。结果 盐酸哌唑嗪的保留时间约为4 . 2min ,且与其它峰的分离度大于1 . 5。盐酸哌唑嗪的线性范围为5~5 0 μg·ml-1 (r=0 . 9999) ,最低检测限为0 .4ng·ml-1 ,平均回收率和RSD分别为1 0 0 .8%和0 . 6 8%。结论 该方法简便、快速,结果准确可靠,适用于盐酸哌唑嗪片的含量及有关物质的定量检测。 相似文献
7.
《Current medical research and opinion》2013,29(9):627-629
SummaryIn a study of10patients sufferingfrom hypertension the results showed that combination treatment with prazosin, cyclopenthiazide and a beta-blocker produced a significant fall in blood pressure. Side-effects such as palpitations, headache, syncope and drowsiness which may occur with prazosin alone were obviated by combining prazosin with a beta-blocker. 相似文献
8.
目的观察去甲肾上腺素(NE)及其α1肾上腺素能受体(α1-AR)拮抗剂哌唑嗪(Prazosin)对自发性高血压大鼠(SHR)动脉血管平滑肌细胞Na -K -ATPase活性及mRNA表达的影响。方法采用生化酶学方法和逆转录聚合酶链反应技术,观察不同浓度的NE和哌唑嗪对自发性高血压大鼠血管平滑肌细胞Na -K -ATPase活性和mRNA表达的影响。结果与SHR组比较,NE(10-7mol/L)能减弱Na -K -ATPase活性(3·98±0·14vs7·92±0·19,P<0·01)及Na -K -ATPaseα1-亚单位mRNA的表达(0·863±0·057vs1·307±0·051,P<0·01),单用哌唑嗪对Na -K -ATPase活性及mRNA的表达均无影响(P>0·05)。哌唑嗪(10-7,10-6,10-5mol/L)呈剂量依赖性减弱和阻断NE(10-7mol/L)对Na -K -ATPase活性(4·31±0·24,6·15±0·30,7·52±0·31)及Na -K -ATPaseα1-亚单位mRNA表达(0·857±0·041,1·096±0·055,1·183±0·059)的影响(P<0·01,P<0·05)。结论NE抑制SHRNa -K -ATPase活性和下调Na -K -ATPaseα1-亚单位mRNA表达,可能是通过α1-AR途径介导基因转录的下调。肾上腺素能1型受体拮抗剂哌唑嗪可通过阻断α1-AR途径抑制NE对自发性高血压大鼠血管平滑肌细胞Na -K -ATPase活性和Na -K -ATPaseα1-亚单位mRNA表达的影响。 相似文献
9.
Loukia Katsouri Marcela P. Vizcaychipi Simon McArthur Ian Harrison Marc Suárez-Calvet Alberto Lleo Dafydd G. Lloyd Daqing Ma Magdalena Sastre 《Neurobiology of aging》2013
Noradrenergic deficits have been described in the hippocampus and the frontal cortex of Alzheimer's disease brains, which are secondary to locus coeruleus degeneration. Locus coeruleus is the brain stem nucleus responsible for synthesis of noradrenaline and from where all noradrenergic neurons project. In addition, it has been suggested that noradrenaline might play a role in modulating inflammatory responses in Alzheimer's disease. In this study we aimed to investigate the effect of various agonists and antagonists for adrenergic receptors on amyloid precursor protein processing. Among them, we found that prazosin, an α1-adrenoceptor antagonist, was able to reduce the generation of amyloid β in N2a cells. Treatment of transgenic APP23 mice with prazosin prevented memory deficits over time. Although prazosin did not influence amyloid plaque load, it induced astrocytic proliferation and increased the release of apolipoprotein E and anti-inflammatory cytokines. These findings suggest that chronic treatment with prazosin leads to an anti-inflammatory response with potential beneficial effects on cognitive performance. 相似文献
10.
The current study was carried out with an attempt to separate similarly structured title drugs by liquid chromatography. Spectrophotometric techniques were generally insufficient under these conditions because of the spectral overlapping of drugs with similar functional groups. The pharmaceutical drugs prazosin, terazosin, and doxazosin contain the same parent quinazoline nucleus, thus making it especially difficult to separate the former two drugs because of their very similar structures. A simple and sensitive method for the routine determination of these drugs in pharmaceutical formulations was attempted. We found that the mobile phase consisting of A: ACN–diethylamine (0.05 ml), B: methanol, and C: 10 mM Ammonium acetate separated these drugs effectively. Separations were carried out on a new Kromasil C18 column (250 × 4.6 mm, 5.0 μm) at 254 nm wavelength. The calibration curve was found to be linear in the range of 2–500 μg/ml. The stated method was then validated in terms of specificity, linearity, precision, and accuracy. Additionally, the proposed method reduced the duration of the analysis. 相似文献