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71.
甲基黄酮醇胺盐酸盐对异丙肾上腺素正性频率作用的影响 总被引:2,自引:0,他引:2
本文比较了甲基黄酮醇胺盐酸盐(MFOA)、普萘洛尔(Pro)、维拉帕米(Ver)对异丙肾上腺素(Iso)所致兔离体右心房正性频率作用的影响。Pro使Iso累积浓度反应曲线平行右移,不抑制最大反应,属于典型的竞争性抑制剂,其pA2=8.43;MFOA和Ver使Iso量效曲线向下右移,抑制最大反应,为非竞争性拮抗。MFOA(2×10~(-5)M)和Ver(2×10~(-7)M)分别使最大反应下降19.28%和48.57%,其pD'2值分别为4.07±0.14、6.68±0.15。结果表明MFOA的作用不同于Pro,和Ver相似。 相似文献
72.
对比观察在自然呼吸、窒息兴奋期和抑制期电针28只麻醉家兔“降压点”穴对动脉血压和积分膈神经放电的影响,经124次实验发现:于上述三种状态下电针耳穴血压下降分别为7.48±0.67kpa(P 0.01)、4.83±0.63kpa和4.25±0.7kpa(p<0.05);积分膈神经放电频率增快为2.87±0.26次/10秒,3.54±0.31次/10秒和3.24±0.41次/10秒(p<0.01)。结果表明电针该穴有显著降压阳增快呼吸频率的作用,其中兴奋期比抑制期降压更为明显。为临床进一步研究耳针对高血压急症和呼吸衰竭的抢救提供了实验资料。 相似文献
73.
用改良的四氮唑硝基蓝(NBT)还原法观察了电针以及生物活性物质(BAS)包括5-羟色胺(5-HT)、血管活性肠肽(VIP)、生长抑素(SOM)和P物质(SP)对大鼠多形核白细胞(PMN)杀菌功能的影响。结果表明:电针及BAS均能增强大鼠PMN的杀菌功能(P<0.01);BAS对大鼠PMN的杀菌功能具有双向调节效应。纳洛酮可阻抑电针对PMN杀菌功能的提高(P>0.05);可被BAS所翻转。电针的镇痛效应和NBT阳性细胞提高效应之间存在着明显的正相关(P<0.01)。 相似文献
74.
培养Wistar大鼠乳鼠的心室肌细胞,向培养基中分别加入浓度为1.56μg/ml至50μg/ml的大豆皂甙,可使心肌细胞群落的自发性搏动呈剂量依赖性抑制。洗脱大豆皂甙或向培养基中再加入10μg/ml肾上腺素均能使自发性搏动恢复。向培养基中加入大豆皂甙5μg/ml使心肌细胞动作电位的波幅、波宽、超射、最大舒张电位、阈电位、最大除极速度等各电参数立即减小。Ca~(2+)80μg/ml能使动作电位的抑制逆转。上述结果表明大豆皂甙对培养的鼠心肌细胞具有钙通道阻滞用。 相似文献
75.
Voltage-Gated calcium channels and nonvoltage-gated calcium uptake pathways in the rat incisor odontoblast plasma membrane 总被引:4,自引:1,他引:3
Odontoblasts participate actively in the transport and accumulation of Ca2+ ions to the mineralization front during dentinogenesis. These cells are known to carry membrane-bound ATP-driven pumps and
Na+/Ca2+ antiports for Ca2+ extrusion, but little is known about Ca2+ influx mechanisms into these cells. It has been shown that the administration of Ca2+ channel blockers in vivo strongly impairs Ca2+ uptake in the mineral phase during dentinogenesis in the rat; the present in vitro study is aimed at further elucidating
odontoblast Ca2+ uptake mechanisms. Dissected rat incisor odontoblasts exhibited a pronounced fluorescence when incubated with a fluorescently-labeled
(STBodipy) dihydropyridine, which is specific for voltage-gated Ca2+ channels of the L-type, and this binding was competitively abolished by nifedipine. As assayed by fluorescence spectrometry,
odontoblast Ca2+ uptake was enhanced by the agonistic dihydropyridine BAYK-8644 (5 μM) as well as by plasma membrane depolarization in a high
K+ (120 mM) medium. The Ca2+ uptake after depolarization was impaired by nifedipine (5 μM). When treated with the Ca2+-ATPase inhibitor cyclopiazonic acid (CPA; 10 μM), a nonvoltage-gated uptake of 45Ca2+ was identified. This uptake was not influenced by nifedipine (20 μM) but was impaired by lanthanum ions (200 μM). A nonvoltage-gated
uptake of Mn2+ into CPA-treated cells could be traced using the fura-2 quenching technique. This CPA-induced Ca2+ flux was not caused by an alteration of the plasma membrane potential, as assayed with di-8-ANEPPS. The results demonstrate
that Ca2+ flux into dentinogenically active odontoblasts occurs through voltage-gated Ca2+ channels of the L-type and by nonvoltage-gated, agonist-sensitive Ca2+ uptake pathways.
Received: 6 November 1995 / Accepted: 21 February 1996 相似文献
76.
电针对大鼠海马兴奋性突触后电位长时程增强的作用 总被引:4,自引:0,他引:4
目的 观察电针对麻醉状态下正常和东莨菪碱引起的学习记忆减退模型大鼠海马突触EPSP长时程增强(LTP)的作用。方法 引导大鼠海马齿状回颗粒细胞层突触后兴奋性电位群(EPSPs),强直刺激(HFS)大脑皮层前穿质区引起海马突触LTP反应;用东莨菪碱制备学习记忆障碍模型;观察电针大椎和肾俞穴对正常和模型大鼠海马LTP的影响。结果 电针对HFS诱发的海马突触LTP效应,其作用强于未电针组,部分参数和时段有统计学意义(P<0.05),且维持时间长于后者;东莨菪碱i.p可显著抑制HFS诱发的海马突触LTP(P<0.01),电针能显著对抗这一抑制作用(P<0.01;P<0.05)。结论 电针对HFS引起的海马突触LTP有一定的易化作用,并对东莨菪碱引起的学习记忆障碍有显著的对抗作用。 相似文献
77.
Angela Ameri 《Naunyn-Schmiedeberg's archives of pharmacology》1997,355(2):273-280
The effects of the Aconitum alkaloid 3-acetylaconitine on neuronal activity were investigated in the slice preparation and on cultivated neurons of rat
hippocampus by extracellular and patch-clamp recordings, respectively. 3-Acetylaconitine (0.01–1 μM) diminished the orthodromic
and antidromic population spike in a concentration-dependent manner. The inhibitory action of the drug was preceded by a transiently
enhanced excitability. The latency of onset of the inhibition was accelerated by increased stimulation frequency, whereas
recovery during washout of the alkaloid was accelerated by decreased stimulation frequency. Moreover, the inhibitory effect
of 3-acetylaconitine was evaluated in two different models of epileptiform activity induced either by blockade of GABA receptors
by bicuculline (10 μM) or by a nominal Mg2+-free bathing medium. In accordance with the activity-dependent mode of action, this compound abolished the synaptically evoked
population spikes in the presence of bicuculline or nominal Mg2+-free bathing medium, respectively. Whole-cell patch-clamp recordings revealed an interaction of 3-acetylaconitine with the
voltage-dependent sodium channel. At a concentration of 1 μM, 3-acetylaconitine did not affect the peak amplitude of the sodium
current, but shifted the current-voltage relationship in the hyperpolarized direction such that sodium currents were already
activated at the resting potential.
Received: 22 July 1996 / Accepted: 14 October 1996 相似文献
78.
吡那地尔对体外培养大鼠大脑皮层神经细胞缺氧缺糖损伤的保护作用 总被引:1,自引:0,他引:1
目的 :探讨ATP敏感性K+ 通道 (KATP)开放剂吡那地尔 (pinacidil,Pin)对缺氧缺糖再复氧损伤大鼠大脑皮层神经细胞的保护作用。方法 :体外培养大鼠大脑皮层神经细胞 ,细胞培养至 10d ,建立神经细胞缺氧缺糖损伤模型 ,观察Pin及KATP阻断剂格列苯脲对缺氧缺糖不同时间 ,再复氧 2 4h后细胞死亡率、丙二醛 (MDA)含量、超氧化物歧化酶 (SOD)活力的影响。结果 :缺氧缺糖、再复氧后大鼠的神经细胞死亡率均显著升高、MDA生成增多、SOD的活力下降 ,Pin干预后 ,细胞死亡率下降、MDA生成减少、SOD的活力升高 ;格列苯脲能拮抗Pin这种保护作用。结论 :Pin对缺氧缺糖损伤神经细胞具有保护作用 ,并与拮抗氧自由基有关 相似文献
79.
Joel A. Black Ruth Westenbroek Bruce R. Ransom William A. Catterall Stephen G. Waxman 《Glia》1994,12(3):219-227
The expression of sodium channel α-subunit isoforms in astrocytes in adult rat spinal cord and optic nerve was examined utilizing immunocytochemical methods with antibodies generated against conserved and subtype-specific sequences of the sodium channel. In adult rat spinal cord, astrocytes within the dorsal and ventral funiculi were immunolabelled with antibody SP20, which recognizes a conserved sequence within sodium channel types I, II, and III. In addition, astrocytes within these spinal cord white matter tracts were immunostained with antibody SP11-II, which recognizes sodium channel type II. Antibodies SP11-I and SP32-III, which are directed against subtype-specific sequences in sodium channel types I and III, respectively, did not label astrocytes in the dorsal and ventral funiculi of the spinal cord. In optic nerves, astrocytes were immunostained with antibody SP20. However, no detectable labelling of cells within the optic nerve was observed with antibodies SP11-I, SP11-II, and SP32-III. These observations demonstrate that sodium channel II is expressed by astrocytes in spinal cord white matter. Moreover, these data suggest that regional factors regulate the level of sodium channel isoform expression in astrocytes. 相似文献
80.