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1.
M. R. Wang C. Y. Chai J. S. Kuof 《Clinical and experimental pharmacology & physiology》1994,21(1):21-29
1. In chloralose-urethane anaesthetized cats, the dorsal cardiovascular reactive area (DCRA) in the parvocellular reticular nucleus dorsomedial to the facial nucleus, and the ventral cardiovascular reactive area (VCRA) ventromedial to the facial nucleus, were stimulated by microinjections of sodium glutamate (100–200 nmol) or electric current. 2. Stimulation of DCRA, with a long latency of 15–20 s, elicited a marked increase of blood flow in the contralateral femoral artery with little change to moderate increase in systemic arterial blood pressure (ABP). In the relatively dorsal portion of DCRA, however, a smaller increase of blood flow in the ipsilateral femoral artery was elicited. 3. On the other hand, stimulation of VCRA with a short latency (3–5 s) evoked an increase of blood flow in both femoral arteries which was more prominent on the contralateral side. The responses were accompanied with decreases in the blood flow of other vascular beds with only a slight increase or minimal change in ABP. 4. The data suggest that DCRA and VCRA are both viscerotopically organized to alter the resistance of individual vascular beds for redistribution of blood flow. 相似文献
2.
大鼠延髓腹外侧区在可乐定心血管效应中的作用 总被引:1,自引:1,他引:0
目的:探讨大鼠延髓腹外侧区(VLM)在介导可乐定心血管效应中的作用。方法:氨基甲酸乙酯麻醉SD大鼠,应用微量注射和细胞外记录等方法观察尾端延髓腹外侧区(CVLM)和头端延髓腹外侧区(RVLM)内局部给予可乐定导致的心血管活动变化。结果:单侧CVLM微量注射可乐定(5nmol/100nl,n=10)不仅能明显升主动脉血压(AP)和增加心率(HR)(P<0.01),而且能增加同侧RVLM压力敏感性神经元(n=80)的放电频率(P<0.01),而单侧RVLM微量注射可乐定(5nmol/100nl,n=9),明显降低AP和HR(P<0.01)。结论:RVLM和CVLM在介导可乐定的心血管效应中具有不同的作用。 相似文献
3.
4.
Fanardzhyan VV Papoyan EV Pogosyan VI Gevorkyan OV 《Neuroscience and behavioral physiology》2002,32(1):53-59
Studies on rats showed that the facilitating influence of preliminary transection of the rubrospinal tract on recovery of motor activity and operant reflexes disrupted by lesioning of the red nucleus was more apparent when lesioning was chemical than when lesioning was electrolytic. This is due to the survival of cerebellothalamic fibers to the ventrolateral nucleus of the thalamus after chemical lesioning of the red nucleus with quinolinic acid. It was also shown that preliminary lesioning of the ventrolateral thalamic nucleus strongly hindered the switching of motor activity under the control of the corticospinal tract in rats subjected to section of the rubrospinal tract and lesioning of the red nucleus. 相似文献
5.
Bilateral intrathalamic microinjections of nanogram amounts (5–50 ng) of muscimol, a γ-aminobutyrate (GABA) receptor agonist, elicited catalepsy in rats. Like neuroleptic-treated rats, those injected with muscimol in the thalamus remained suspended on a vertical grid but, unlike opioid-treated rats, they failed to remain horizontal on two book-holders. The righting reflex was present, while ptosis was absent. The areas with the highest sensitivity to the cataleptogenic effects of muscimol were the ventromedial and ventral-anterior nuclei of the thalamus. These thalamic areas were also characterized by the shortest latency for the induction of catalepsy. Injection of up to 50 ng of muscimol into the caudate, globus pallidus or entopeduncular nucleus failed to produce catalepsy. Catalepsy was also obtained after intrathalamic microinjection of other GABA analogs, such as 3-aminopropanesulphonic and imidazolacetic acid, which are known to be potent GABA receptor agonists, and β-p-chlorophenyl-GABA , a compound which has GABA mimetic activity. The catalepsy produced by 10 ng of muscimol was reversed by an intrathalamic microinjection of picrotoxin, a GABA receptor antagonist. Muscimol-induced catalepsy, unlike neuroleptic-induced catalepsy, was not reversed by systemic administration of high doses of apomorphine, a dopamine receptor agonist, or of scopolamine, a muscarine antagonist, or by intranigral injection of muscimol, and was not prevented by kainic acid-induced lesions of the striatum or of the nigra. Vice versa, injection of cataleptogenic doses of muscimol in the thalamus failed to prevent the stereotyped gnawing produced by systemic apomorphine or intranigral muscimol. Therefore, in these animals, catalepsy and stereotyped gnawing coexisted. The unilateral intrathalamic microinjection of muscimol resulted in a postural asymmetry consisting of turning towards the injected side. This ipsilateral posturing was converted into an ipsilateral circling by systemic administration of apomorphine.The results indicate that thalamic GABAergic mechanisms play an important role in the regulation of posture and in the mediation of certain motor responses arising in the striatum. 相似文献
6.
Frequency-coded impulses are known to be converted into postsynaptic potentials (PSPs) at the synapse of a target neuron. This can be termed frequency-voltage (F-V) conversion. Studies on this problem in pyramidal tract neurons (PTNs) showed that not only the amplitude but also the duration of depolarizing PSPs was determined as a function of the input impulse frequency. Two opposite patterns of F-V conversion were observed following activation of two input systems to PTNs. Inhibitory postsynaptic potentials were found to play an important role in the regulation of the duration of PSPs by curtailing excitatory post-synaptic potentials. 相似文献
7.
Akiko Arata H. Onimaru Ikuo Homma 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1998,119(4):399-408
We analysed the modulation of respiratory neurons by adrenaline or noradrenaline (NA) in a newborn rat brainstem-spinal cord
preparation. Adrenaline or NA caused a dose-dependent depression of the respiratory rhythm and induced C4 spinal tonic discharges.
The inhibitory effect of adrenaline (ED50=0.5 μM) on the respiratory rhythm was stronger than NA (ED50=5 μM). The adrenaline respiratory rhythm depression was partially blocked by the α1-antagonist prazosin or by the α2-antagonist yohimbine. The C4 tonic discharge elicited by adrenaline was blocked by the α1-antagonist prazosin. The direct effects of adrenaline on pre-inspiratory (Pre-I) neurons were examined in a synaptic blockade
solution (low Ca), and fifty-six percent of Pre-I neurons were found to continue firing. In low-Ca solution, Pre-I neurons
were excited (n=29 of 39) or depressed (n=5 of 39) by adrenaline, and excited by α1-agonist phenylephrine or depressed by α2-agonist clonidine. These results suggest that the respiratory rhythm depression under intact network conditions is mediated
by some other inhibitory system. The inhibitory effect of adrenaline on the respiratory rhythm was partially blocked by the
GABAA-antagonists bicuculline or picrotoxin, but not by the GABAB-antagonist phaclofen. The present results suggest that: (1) respiratory rhythm generation is more sensitive to adrenaline
than NA through α-adrenergic action of adrenaline; (2) the activity of Pre-I neurons could be directly regulated by excitation
via α1-receptors and inhibition via α2-receptors; and (3) the depression of the respiratory rhythm by adrenaline is partly mediated by GABAAergic neurons.
Received: 8 April 1997 / Accepted: 6 October 1997 相似文献
8.
大鼠头端延髓腹外侧区NMDA受体在动脉压力感受器反射中的作用 总被引:2,自引:1,他引:1
目的:研究大鼠头端延髓腹外侧区(RVLM)谷氨酸NMDA受体在介导动脉压力感受器反射(ABR)中的作用。方法:在氨基甲酸乙酯麻醉的大鼠RVLM双侧各微注射0.1μ1的50mol/L,氯胺酮,观察动脉血压,心率以及ABR的变化。结果:双侧RVLM内微注射氯胺酮后动脉血压和心率明显下降(P〈0.05),同时能部分或完全阻断ABR(P〈0.05)。结论:谷氨酸NMDA受体在维持交感心血管活动的紧张性兴奋 相似文献
9.
延髓血管压迫致高血压的犬模型 总被引:1,自引:0,他引:1
为制备延髓血管压迫致高血压模型,将12只杂种犬随机均分为模型组和对照组,采用带蒂大网膜移植法,将裁剪好的大网膜经皮下隧道移植至左侧延髓腹外侧及Ⅸ、Ⅹ颅神经入脑干区(REZ),利用大网膜与延髓表面蛛网膜及软脑膜间形成的血管吻合,造成延髓血管压迫;对照组犬的大网膜移植于其小脑表面。结果,模型组术后血压较术前明显升高(P<0.01),对照组血压无明显改变,提示原发性高血压与左侧延髓腹外侧受血管压迫有关。 相似文献
10.
Geoffrey A Head 《Clinical and experimental pharmacology & physiology》1996,23(Z3):93-98
- 1 In a number of species, high concentrations of angiotensin II (AngII) receptors have been found in the rostral ventrolateral medulla (RVLM) in the hindbrain, which is an important region involved in the modulation of sympathetic vasomotor tone. The present review describes studies in which the contribution of angiotensin receptors in the brainstem to cardiovascular regulation, in particular sympathetic vasomotor reflexes, has been examined in conscious and anaesthetized rabbits.
- 2 In conscious rabbits, fourth ventricular infusions of AngII produced dose-dependent pressor responses as doses 400 times less than equipressor intravenous doses. Chronic baroreceptor denervation increased the sensitivity to AngII by 1000-fold. Administration of prazosin i.v. blocked the pressor response, suggesting that the mechanism involved sympathetic vasoconstriction.
- 3 The pattern of haemodynamic changes in response to AngII injected into the fourth ventricle (4V) involved decreased total peripheral conductance and mesenteric conductance, but a rise in hindlimb conductance. Sinoaortic denervation changed the hindlimb fall in conductance to an increase, suggesting that muscle vasomotor pathways were particularly inhibited by baroreceptor feedback mechanisms.
- 4 In anaesthetized rabbits, infusion of AngII into the RVLM increased blood pressure and transiently increased resting renal sympathetic nerve activity. The renal sympathetic baroreflex curves were shifted to the right and the upper plateau of the sympathetic reflex increase was markedly increased.
- 5 The pressor actions of 4V AngII were blocked by administration of a peptide antagonist injected into the RVLM or by the angiotensin AT1 antagonist losartan injected into the 4V. These results suggest that mainly AT1 receptors are involved and that the RVLM is a likely candidate site for the modulation of the renal sympathetic baroreflex.
- 6 Losartan administration into the 4V in conscious rabbits increased resting renal sympathetic tone and enhanced renal sympathetic baroreflex and chemoreflexes.
- 7 Our studies suggest that there are sympathoexcitatory AT1 receptors in the RVLM accessible to AngII from the cerebrospinal fluid. In addition, an AT1 receptor pathway normally inhibits the sympathoexcitation produced by baroreceptor unloading or chemoreceptor activation. The effect of losartan suggests that there is greater tonic activity within the sympathoinhibitory pathways. These two actions suggest that angiotensin receptors in the brainstem modulate sympathetic responses to specific afferent inputs, thus forming part of a potentially important mechanism for the integration of characteristic autonomic response patterns.