全文获取类型
收费全文 | 8936篇 |
免费 | 936篇 |
国内免费 | 200篇 |
专业分类
耳鼻咽喉 | 42篇 |
儿科学 | 52篇 |
妇产科学 | 23篇 |
基础医学 | 1270篇 |
口腔科学 | 213篇 |
临床医学 | 958篇 |
内科学 | 2035篇 |
皮肤病学 | 80篇 |
神经病学 | 1353篇 |
特种医学 | 255篇 |
外国民族医学 | 1篇 |
外科学 | 583篇 |
综合类 | 1003篇 |
现状与发展 | 1篇 |
预防医学 | 720篇 |
眼科学 | 86篇 |
药学 | 1056篇 |
10篇 | |
中国医学 | 225篇 |
肿瘤学 | 106篇 |
出版年
2024年 | 16篇 |
2023年 | 141篇 |
2022年 | 206篇 |
2021年 | 470篇 |
2020年 | 400篇 |
2019年 | 440篇 |
2018年 | 364篇 |
2017年 | 313篇 |
2016年 | 299篇 |
2015年 | 273篇 |
2014年 | 462篇 |
2013年 | 522篇 |
2012年 | 417篇 |
2011年 | 459篇 |
2010年 | 404篇 |
2009年 | 354篇 |
2008年 | 393篇 |
2007年 | 388篇 |
2006年 | 334篇 |
2005年 | 309篇 |
2004年 | 317篇 |
2003年 | 261篇 |
2002年 | 213篇 |
2001年 | 185篇 |
2000年 | 177篇 |
1999年 | 179篇 |
1998年 | 187篇 |
1997年 | 191篇 |
1996年 | 147篇 |
1995年 | 140篇 |
1994年 | 144篇 |
1993年 | 115篇 |
1992年 | 93篇 |
1991年 | 90篇 |
1990年 | 76篇 |
1989年 | 57篇 |
1988年 | 72篇 |
1987年 | 54篇 |
1986年 | 48篇 |
1985年 | 65篇 |
1984年 | 43篇 |
1983年 | 36篇 |
1982年 | 45篇 |
1981年 | 40篇 |
1980年 | 31篇 |
1979年 | 29篇 |
1978年 | 17篇 |
1977年 | 14篇 |
1976年 | 17篇 |
1975年 | 9篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
51.
Pacemaker Current if. Since the hyperpolarization-activated current, if, was originally associated with the diastolic depolarization phase of action potential in the sinoatrial (SA) node in 1979, its central role in the generation and control of pacemaker activity has become increasingly clear through a series of experimental findings, some of which have substantially modified the pre-existing theories of cardiac pacemaking and its modulation by the autonomic transmitters. Thus, the pacemaker current of Purkinje fibers, formerly described as a deactivating pure potassium (K) current, was found to be in fact, like the nodal if, inward and activating on hyperpolarization. Furthermore, in SA node cells, as well as mediating rhythm acceleration induced by catecholamines, if was found to underlie the slowing effect of low acetylcholine (ACh) concentrations, in contrast with the generally accepted hypothesis that activation of a K conductance is the main process responsible for cardiac slowing. A final, atypical property of if recently demonstrated concerns the activating action exerted on if by intracellular cAMP. Unlike that on other voltage-gated, cAMP-modulated cardiac channels, this action is independent of phosphorylation and involves a direct binding of cAMP to if channels. (J Cardiovasc Electrophysiol, Vol. 3, pp. 334–344, August 1992) 相似文献
52.
53.
Reliability of a Core Competency Checklist Assessment in the Emergency Department: The Standardized Direct Observation Assessment Tool 总被引:2,自引:1,他引:1
54.
Tomohiko Ai M. Horie Kazuhiko Obayashi Shigetake Sasayama 《Pflügers Archiv : European journal of physiology》1998,436(2):168-174
To examine mechanism(s) underlying the accentuated antagonism by angiotensin II (A-II) on twitch tension, we recorded L-type
Ca2+ currents (I
Ca,L) using conventional patch-clamp techniques in single, guinea-pig, ventricular myocytes. I
Ca,L was recorded by a step-pulse protocol after eliminating K+ conductances (internal Cs+ plus tetraethylammonium chloride and K+-free extracellular solution). A-II (100 nM) did not affect basal I
Ca,L, but inhibited I
Ca,L that had been enhanced (approximately 200% of control) by (ISO, isoproterenol 100 nM). The inhibitory action of A-II was
concentration dependent (concentration eliciting 50% inhibition 88±9 pM, n=41) and the ISO-enhanced component of I
Ca,L was completely blocked by A-II at concentrations above 10 nM. CV-11974 (500 nM), an A-II type-1 receptor (AT1) antagonist, prevented the inhibitory action of A-II. Pre-incubation with pertussis toxin (PTX) abolished the inhibitory
effect of A-II. A-II also inhibited the I
Ca,L enhanced by histamine (500 nM) and forskolin (1 μM), but failed to affect I
Ca,L enhanced by intracellular cyclic adenosine monophosphate (1 mM). The inhibitory action of A-II may therefore involve AT1 receptors/PTX-sensitive, guanine nucleotide-binding (G) proteins (Gi)/adenylate cyclase and partially explains the A-II-dependent
accentuated antagonism of inotropy. 相似文献
55.
导管射频消融治疗房室结折返性心动过速前后心率变异的改变 总被引:1,自引:0,他引:1
对20例房室结折返性心动过速患者在射频消融前后进行心率变异频域和时域分析,以了解射频消融对心脏自主神经系统的影响。结果显示,心率变异的极低频段(ULFP)、低频段(LFP)、高频段(HFP)及总能谱(TFP)均较射频消融前降低(P〈0.05)。提示射频消融对心脏交感神经、融交感神经均有损害,而以副交感神经损害为主。 相似文献
56.
The potassium conductance increased by BRL 34915 (BRL, cromakalim) was studied in single guinea pig ventricular myocytes by using a whole cell voltage-clamp technique. In control voltage-clamp recordings, the late current-voltage relation showed a distinct inward rectification. BRL (1–100 μM) shortened the action potential and diminished or abolished inward rectification but had no effect on the slope conductance and currents flowing during hyperpolarizing clamp steps. BRL did not decrease the slow inward current but accelerated the time constant of activation and amplitude of the outward current. Cd markedly decreased (0.2 mM) or abolished (0.4–0.6 mM) the slow inward current and BRL induced a faster outward shift of late current to a greater value. Glybenclamide (10 μM), a blocker of ATP-sensitive K+ channels, had little effect of its own on action potential, membrane currents, and I-V relation. However, in the presence of BRL, glybenclamide abolished BRL effects on action potential and currents and restored inward rectification. It is concluded that the mechanism by which BRL shortens the action potential is a faster growth of an outward current due to the reduction or abolition of the inward rectification of an ATP-dependent potassium channel. The reduction in force in non-isolated tissues appears to be an indirect result of the action potential shortening and not of a decreased slow inward current. 相似文献
57.
1. The effect of strophanthidin on the slow inward current (Isi) and on contractile force were studied in guinea-pig isolated ventricular myocytes and intact papillary muscles, respectively. In myocytes, both low (10 nmol/L) and high (1-10 mumols/L) concentrations had small or no effects in either direction on Isi whereas norepinephrine (10-100 nmol/L) increased it. To determine whether the same results are obtained after decreasing or increasing intracellular calcium or sodium, the same concentrations of strophanthidin were tested in different procedures that are known to (i) increase [Ca]i and decrease [Na]i (high [Ca]o, 3.6-5.4 mmol/L; low [Na]o, 112 mmol/L; (ii) decrease [Ca]i and increase [Na]i (low [Ca]o, 0.45-1 mmol/L; Sr, 1 mmol/L; (iii) decrease [Ca]i and [Na]i (Cd, 0.1-0.2 mmol/L); and (iv) increase [Ca]i and [Na]i (veratridine, 0.2 mumol/L). High [Ca]o and veratridine increased whereas low [Ca]o and Cd decreased Isi. In contrast, during these various procedures, strophanthidin had small and inconsistent effects at a low or high concentration. In intact papillary muscles, low strophanthidin decreased whereas high strophanthidin increased contractile force. It is concluded that strophanthidin has little direct or indirect effect on Isi and that the decrease in force by low and increase in force by high concentrations in intact muscle are probably related to demonstrated decrease and increase, respectively, in intracellular sodium activity. 相似文献
58.
59.
Effects of nilvadipine on the low- and high-voltage activated Ca2+ currents (LVA and HVA ICa, respectively) were compared with other organic Ca2+ antagonists in acutely dissociated rat hippocampal CA1 pyramidal neurons. The inhibitory effects of nilvadipine, amlodipine and flunarizine on LVA ICa were concentration- and use-dependent. The apparent half-maximum inhibitory concentrations (IC50s) at every 1- and 30-s stimulation were 6.3×10−7 M and 1.8×10−6 M for flunarizine, 1.9×10−6 M and 7.6×10−6 M for nilvadipine, and 4.0×10−6 M and 8.0×10−6 M for amlodipine, respectively. Thus, the strength of the use-dependence was in the sequence of nilvadipine>flunarizine>amlodipine. Nilvadipine also inhibited the HVA ICa in a concentration-dependent manner with an IC50 of 1.5×10−7 M. The hippocampal CA1 neurons were observed to have five pharmacologically distinct HVA Ca2+ channel subtypes consisting of L-, N-, P-, Q- and R-types. Nilvadipine selectively inhibited the L-type Ca2+ channel current which comprised 34% of the total HVA ICa. On the other hand, amlodipine non-selectively inhibited the HVA Ca2+ channel subtypes. These results suggest that the inhibitory effect of nilvadipine on the neuronal Ca2+ influx through both LVA and HVA L-type Ca2+ channels, in combination with the cerebral vasodilatory action, may prevent neuronal damage during ischemia. 相似文献
60.
The actions of the nonsteroidal antiinflammatory drug niflumic acid were studied on frog neuromuscular preparations by conventional electrophysiological techniques. Niflumic acid reduced the amplitude and increased the latency of endplate potentials in a concentration-dependent manner. Neuromuscular junctions pretreated with niflumic acid (0.05–0.5 mM) showed much less depression than control when they were stimulated with trains of impulses. Inhibition of acetylcholine release was reverted by raising the extracellular Ca2+ concentration but not by simply washing out the preparations with niflumic acid-free solutions. Pretreatment with indomethacin (0.1 mM), another nonsteroidal antiinflamatory drug, did not affect the niflumic acid-induced inhibition of evoked responses. Niflumic acid (0.1 mM) did not change the amplitude of miniature endplate potentials and had a dual action on the frequency of miniatures: it decreased their frequency at 0.1 mM whereas it produced an enormous increase in the rate of spontaneous discharge at 0.5 mM. Niflumic acid (0.1–1 mM) reversibly increased the amplitude and affected the kinetics of presynaptic voltage-activated K+ current and Ca2+-activated K+ current in a concentration-dependent manner. Niflumic acid (0.1–1 mM) irreversibly decreased the amplitude and reversibly affected the kinetics of the nodal Na+ current. Indomethacin (0.1 mM) had no effect on presynaptic currents. In conclusion, niflumic acid reduces acetylcholine release by increasing presynaptic K+ currents. This may shorten the depolarizing phase of the presynaptic action potential and may reduce the entry of Ca2+ with each impulse. 相似文献