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101.
B. Larsson E. D. Högestätt A. Mattiasson K. -E. Andersson 《Naunyn-Schmiedeberg's archives of pharmacology》1984,326(1):14-21
Summary In order to study differences in action between Ca2+-entry blockers on smooth muscle and peripheral nerves, the effects of nifedipine, verapamil, and diltiazem on noradrenaline (NA)-induced contractions and electrically evoked release of 3H-NA were investigated in the female rabbit urethra. In addition, possible influences of Ca2+-entry blockers on alpha-adrenoceptors were studied with radioligand binding technique. Exposure to Ca2+-free medium completely abolished the contractile response to 1 M NA in the rabbit urethra, indicating that the contraction was entirely dependent on influx of extracellular Ca2+. The Ca2+-entry blockers inhibited the NA-induced contractions in the following order of potency: nifedipine>verapamildiltiazem. In contrast to nifedipine and diltiazem, which produced a maximum inhibition of between 50 and 60%, verapamil was able to abolish the contractile responses to NA. The electrically evoked efflux of 3H-NA was decreased by diltiazem and increased by verapamil, whereas nifedipine failed to alter the 3H-NA efflux. Only verapamil was effective in inhibiting specific 3H-DHE binding to a crude membrane preparation of the rabbit bladder base and urethra, and the inhibition appeared to be of the competitive type. It is suggested that the effects of verapamil on electrically evoked efflux of 3H-NA and on NA-induced contractions can be partly explained by blockade of pre- and post-junctional alpha-adrenoceptors. The failure of nifedipine and diltiazem to abolish the NA-induced contraction might indicate the existence of different Ca2+-entry pathways in urethral smooth muscle. 相似文献
102.
脉络宁对骨内高压血液流变学的影响 总被引:2,自引:0,他引:2
目的 观察脉络宁对骨内高压时血液流变学指标的影响。方法 将家兔一侧后肢于膝关节伸直接固定5周,造成固定侧胫骨上端骨内高压模型,测定血液流变学指标,与静脉注射脉络宁2周后血液流变学指标进行比较。结果 骨内高压时全身静脉血和骨髓血粘度均明显升高;给予脉络宁治疗2周后,其静脉血和骨髓血粘度明显降低,同正常组相比差异无显著性(P>0.05)。同时,骨内压明显下降。结论 脉络宁可通过改善全身和局部血液流变学指标,纠正骨内循环动力异常,降低骨内高压。 相似文献
103.
104.
C. R. Caflisch S. Solomon W. R. Galey 《Pflügers Archiv : European journal of physiology》1979,380(2):121-125
An improvedpCO2 microelectrode has been evaluated and used to investigate whether a significant barrier to diffusion of CO2 exists in the rabbit pancreas. The results of this study show the improved Carter and CaflischpCO2 microelectrode to be an accurate and reliable tool for measuring pancreatic venous and ductalpCO2. The similarities betweenpCO2 values from the pancreatic ducts and small pancreatic veins suggest that there is no barrier to CO2 diffusion between small veins and exocrine ducts in the rabbit pancreas, and that ductalpCO2 is probably strongly influenced by the CO2 tension of the small pancreatic blood vessels. 相似文献
105.
106.
107.
A. Hirose R. Tsuji H. Shimizu T. Tatsuno H. Tanaka Y. Kumasaka M. Nakamura 《Naunyn-Schmiedeberg's archives of pharmacology》1990,341(1-2):8-13
Summary Electrophysiological studies using spectral analysis techniques were undertaken in rabbits to determine whether or not hippocampal rhythmical slow activity (RSA, theta wave activity) was affected by the 5-hydroxytryptamine1A (5-HT1A) agonists 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) and 3 , 4 , 7 , 7 -hexahydro-2-(4-(4-(2-pyrimidinyl)-1-piperazinyl)-butyl)-4, 7-methano-IH-isoindole-1,3(2H)-dione dihydrogen citrate (SM-3997, a newly synthesized anxiolytic drug). Intravenous administration of 8-OH-DPAT and SM-3997 induced a desynchronized pattern with low-amplitude slow wave activity in the hippocampal EEG and inhibited RSA generation following stimulation of the midbrain reticular formation. RSA was also inhibited by 5-HT1A related anxiolytics such as buspirone, gepirone, and ipsapirone. The effects of 8-OH-DPAT and SM-3997 on the hippocampal RSA were blocked by pindolol, which has 5-HT1A antagonistic activity. Direct microinjection of these 5-HTIA selective agonists into the hippocampus inhibited generation of the hippocampal RSA. These findings indicated that 8-OH-DPAT and SM-3997 inhibited the hippocampal RSA by acting on hippocampal 5-HTIA receptors.
Send offprint requests to A. Hirose at the above address 相似文献
108.
Summary Experiments were carried out to elucidate the mechanism that the positive inotropic effect mediated by 1-adrenoceptors is more susceptible to organic calcium antagonists than the -adrenoceptor-mediated effect. Verapamil and diltiazem displaced the specific binding of [3H]prazosin to the membrane fraction derived from the rabbit ventricular myocardium, verapamil being about 70 times more potent than diltiazem. Nifedipine did not displace the binding. While these compounds suppressed the positive inotropic effect mediated via l-adrenoceptors in 1- concentration-dependent manner, there was no correlation between the potency of the compounds to displace the [3H]prazosin binding and to inhibit the -mediated positive inotropic effect. The relative potency of three calcium antagonists to decrease the basal force of contraction and the al-mediated effect (of the same extent as compared to basal force of contraction) was consistent to each other. The positive inotropic effect mediated by -adrenoceptors was inhibited much less, and was enhanced by low concentrations of organic calcium antagonists. The differential action of calcium antagonists on the - and -mediated positive inotropic effect was mimicked by lowering the extracellular calcium concentration to 1/2, 1/4 and 1/8 of that in normal Krebs-Henseleit solution (2.5 mmol/l). These results indicate that the 1-adrenoceptor blocking activity does not play an essential role for the preferential inhibition of -mediated positive inotropic effect by organic calcium antagonists. Difference in the subcellular mechanism involved in mobilization of intracellular Ca2+ subsequent to 1-and -adrenoceptor activation may be responsible for the differential inhibitory action of calcium antagonists in the rabbit heart.
Send offprint requests to M. Endoh at the above address 相似文献
109.
Summary Depolarization and reduction in the C fibre compound action potential (C spike) in response to 5-HT were recorded simultaneously from rabbit isolated vagus nerve. 5-HT (0.1–100 mol/l) was applied either as single concentrations or cumulatively and EC50 and IC50 values measured from individual concentration-response curves. The EC50 values for depolarization (cumulative curves: 2.33, 1.64–3.33 mol/l, geometric means and 95% confidence limits, n = 31; non-cumulative curves: 3.99, 2.89 – 5.52 mol/l, n = 9) were significantly higher than IC50 values for C spike reduction (cumulative curves: 1.25, 0.91–1.74 mol/l, n = 30; non-cumulative curves: 1.41, 0.72–2.76 mol/l, n = 8). Complex effects on the C spike were observed, suggesting a susceptible group of C fibres and a 5-HT-resistant component to the C fibre action potential. The motor nerve C fibres in the vagus nerve appear insensitive to 5-HT, whereas the sensory C fibres were sensitive to 5-HT. Phenylbiguanide had a similar selective effect on the C spike, while the depolarizing agents, 1,1-dimethyl-4-phenylpiperazinium (DMPP) and gamma-aminobutyric acid (GABA) did not. Cumulative concentration-response curves for depolarization and C spike reduction could be repeated reproducibly if an interval of 90 min was left between determinations. Up to 6 curves could be generated from one preparation. The 5-HT uptake inhibitor, citalopram (0.1 and 1 mol/l), had no effect on cumulative concentration-response curves. Concentration-response curves from pooled data, when 5-HT was applied non-cumulatively, showed higher maxima for both depolarization and C spike reduction compared to similar curves for cumulative application of increasing concentrations of 5-HT. It is concluded that although the two actions of 5-HT on the rabbit vagus nerve (depolarization, C spike reduction) closely parallel each other in respect of their cumulative and non-cumulative concentration-response curves, the repeatability of concentration-response curves, and, as reported in a companion paper, blockade by metoclopramide or BRL 43694 and involvement of 5-HT3 receptors, some differences remain which may or may not indicate an independent genesis of the two responses.Send offprint requests to D. I. Wallis at the above address 相似文献
110.
Summary Uridine 5-triphosphate- (UTP-) and adenosine 5-triphosphate-(ATP) induced vasoconstriction was studied in the rabbit basilar artery. The arteries were incubated and perfused at a constant rate of flow. Vasoconstriction was measured as an increase in perfusion pressure.Serotonin, histamine and noradrenaline caused concentration-dependent vasoconstriction, with potency decreasing in that order. Of the nucleotides tested, UTP, UDP, UMP, CTP, ATP, ADP, adenosine 5-O-(3-thio)triphosphate (ATPS), and ,-imido adenosine 5-triphosphate (AMP-PNP) elicited concentration-dependent vasoconstriction, whereas AMP, 2-methylthio-ATP, , -methylene-ATP and ,-methylene-ATP up to 10–3 mol/l caused no or only a very small increase in perfusion pressure. The order of potency of the pyrimidine nucleotides was: UTP = UDP UMP = CTP; that of the purine nucleotides was: ATPS > AMP-PNP > ATP > ADP > 2-methylthio-ATP = , -methylene-ATP = ,-methylene-ATP. The vasoconstrictor effects of UTP and ATP were not or only to a minor degree influenced by: phentolamine; a mixture of atropine, diphenhydramine and methysergide; indometacin; nordihydroguaiaretic acid; denervation by 6-hydroxydopamine; or mechanical removal of endothelium. Prolonged exposure to ,-methylene-ATP elicited only a very small vasoconstriction and did not change the constrictor effects of UTP or ATP. Prolonged exposure to ATPS elicited marked vasoconstriction; subsequently, responses to ATP were reduced whereas those to UTP were, if anything, slightly enhanced. Reactive blue 2 reduced neither the UTP- nor the ATP-induced vasoconstriction. ATP 10–3 mol/l elicited marked additional vasoconstriction after precontraction with UTP 10–3 mol/l, whereas UTP elicited only a very small additional vasoconstriction when its concentration was doubled from 10–3 to 2 × 10–3 mol/l.It is concluded that, in the rabbit basilar artery, the vasoconstrictor response to UTP is mediated by a pyrimidine nucleotide receptor which is distinct from the P2-purinoceptor, and that the vasoconstrictor response to ATP is mediated by a P2-receptor which is distinct from the known P2-subtypes.Send offprint requests to I. v. Kügelgen at the above address 相似文献