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91.
目的探讨食管多通道腔内阻抗技术联合pH检测对嗳气症各亚型的发病机制及临床疗效。方法以我院2009年8月至2011年8月治疗的128例嗳气症患者为研究对象,使用食管多通道腔内阻抗技术联合pH检测进行检测,对嗳气患者各亚型的发病机制、与胃食管反流的关系等进行研究;使用巴氯芬对研究对象进行治疗,并进行各亚型之间的疗效比较,并对相关数据进行统计学分析。结果通过食管多通道腔内阻抗联合pH监测发现:①吞气症和非特异性嗳气综合征的发病机制不同,吞气症的嗳气是由气体吞咽后,且所吞咽的气体并未进入胃内而引发症状,非特异性嗳气综合征则是由胃内引发,且不伴有吞咽;②胃食管反流与嗳气发生的时间具有相关性,吞气症可能是由于瞬间下食管括约肌的松弛导致嗳气和反流同时发生,非特异性嗳气综合征可能是嗳气发生后由于LES的松弛导致反流的发生;③使用巴氯芬治疗,非特异性嗳气综合征的疗效优于吞气症,差异具有统计学意义(P>0.05)。结论嗳气症各型的发病机制不同,直接导致使用巴氯芬治疗的效果存在差异性;胃食管炎与嗳气症存在时间相关性,吞气症可能是由于瞬间下食管括约肌的松弛导致嗳气和反流同时发生,非特异性嗳气综合征可能是嗳气发生后由于LES的松弛导致反流的发生。 相似文献
92.
93.
GABA mechanisms in the pedunculopontine tegmental nucleus influence particular aspects of nicotine self-administration selectively in the rat 总被引:7,自引:7,他引:0
William A. Corrigall Kathleen M. Coen Jianhua Zhang Laurel K. Adamson 《Psychopharmacology》2001,158(2):190-197
RATIONALE: The pedunculopontine tegmental nucleus (PPTg) is part of the neuronal circuit activated by self-administered nicotine. The cholinergic neurons of the PPTg comprise a prominent projection to midbrain dopamine neurons. However, anatomical studies of Fos expression suggest that nicotine targets primarily non-cholinergic neurons in the PPTg, especially GABAergic and glutamatergic neurons. OBJECTIVE: The objective of these experiments was to examine the role of GABA manipulations in the PPTg on nicotine self-administration. METHODS AND RESULTS: Rats trained to self-administer nicotine or cocaine intravenously were prepared with brain microcannulae directed to the PPTg. Intra-PPTg microinfusions of the GABA agonists muscimol (10-50 ng) and baclofen (30-60 ng) reduced nicotine self-administration maintained on a fixed-ratio schedule of reinforcement (30 microg/kg per infusion); self-administration of cocaine (0.3 mg/kg per infusion) under an identical schedule was not affected. Muscimol and baclofen were also examined after intra-PPTg microinfusion in animals trained to self-administer nicotine on a progressive-ratio schedule (10 and 30 microg/kg per infusion). Progressive-ratio responding was sensitive to pharmacological manipulations such as a change in the nicotine dose available for self-administration, or intra-PPTg microinfusion of the nicotinic antagonist dihydro-beta-erythroidine (30 microg). However, nicotine self-administration on a progressive-ratio schedule was not altered by intra-PPTg microinfusions of GABA agonists. CONCLUSIONS: These data confirm that the PPTg is involved in nicotine self-administration, a conclusion that is independent of the schedule of reinforcement that is used. GABAergic mechanisms in the PPTg play a selective role in nicotine reinforcement compared to cocaine, and that role is restricted to the characteristics of reinforcement measured by fixed-ratio responding. 相似文献
94.
γ-Aminobutyric acid (GABA) is a principal inhibitory neurotransmitter in vertebrate nervous system. The metabotropic receptor for GABA, GABAB receptor, is characterized as a G protein-coupled receptor subtype. In the present study, GABAB receptor-like immunoreactivity (GABABR-LI) in the rat spinal cord and dorsal root ganglion (DRG), as well as GABAB receptor-mediated depression in the spinal dorsal horn were examined by using immunohistochemistry and whole-cell voltage-clamp recording technique, respectively. Under light microscope, GABABR-LI was densely found in laminae I and II of the dorsal horn. DRG cells of various diameters also showed GABABR-LI. Electron microscopy further revealed that GABABR-LI was also localized in terminals of myelinated, unmyelinated fibers as well as the somatodendritic sites of dorsal horn neurons. Bath application of a GABAB receptor agonist, baclofen (10 μM, 30 s), induced a slow outward (inhibitory) current in dorsal horn neurons. This slow current was depressed when the postsynaptic G protein-coupled receptor was inhibited, indicating the postsynaptic action of baclofen. Under the condition of postsynaptic GABAB receptor being inhibited, baclofen (10 μM, 60 s) depressed large (Aβ) and fine (C, Aδ) afferent fiber-evoked monosynaptic excitatory postsynaptic currents, indicating presynaptic inhibition of GABAB receptor on elicited neurotransmitter release. Taken together, the results suggest that baclofen-sensitive GABAB receptor is expressed pre- and postsynaptically on primary afferent fibers and neurons in the spinal dorsal horn; activation of GABAB receptor in the dorsal horn postsynaptically hyperpolarizes dorsal horn neurons and presynaptically inhibits primary afferents. 相似文献
95.
96.
Adenosine is acknowledged to have a primarily inhibitory function in the central nervous system, but is believed to have little effect on inhibitory neurones themselves. It is however, difficult to determine the effect of adenosine on inhibitory synaptic potentials since adenosine directly depresses evoked potentials and, in the presence of bicuculline to block GABAA-mediated inhibition, the bicuculline-resistant fraction of paired-pulse inhibition (ppi) is greater between pairs of small potentials than between pairs of larger potentials. Here, adenosine increased bicuculline-resistant ppi when stimulus strength was constant between adenosine and control but ppi of responses in adenosine was markedly less than ppi of control responses of the same size. Adenosine had less effect on the size of ‘conditioned’ potentials than on control potentials. It is concluded that adenosine can reduce the bicuculline-resistant fraction of paired-pulse inhibition in the hippocampus. Further quantitative comparison of the effects of adenosine on ppi and on single evoked potentials excluded a difference in the potency of adenosine at excitatory and inhibitory terminals as an explanation for this activity. The results suggest that adenosine may diminish bicuculline-resistant paired-pulse inhibition by enhancing a simultaneous facilitatory component of the neuronal responses. 相似文献
97.
James L. McGaugh Ines B. Introini-Collison Alan H. Nagahara Larry Cahill Jorge D. Brioni Claudio Castellano 《Neuroscience and biobehavioral reviews》1990,14(4):425-431
Neuromodulatory systems activated by training experiences appear to play a role in influencing memory storage processes. The research summarized in this paper examined the effects, on memory, of posttraining administration of treatments affecting adrenergic, opioid peptidergic and GABAergic systems. When administered after training, drugs affecting these systems all produce dose- and time-dependent effects on memory storage. The drug effects on memory are blocked by lesions of the amygdaloid complex as well as lesions of the stria terminalis, a major amygdala pathway. The effects of drugs affecting these neuromodulatory systems are also blocked by injections of beta-adrenergic antagonists administered to the amygdaloid complex. Thus, the findings suggest that the neuromodulatory systems affect memory storage through influences involving the activation of beta-adrenergic receptors within the amygdala. These findings are consistent with the view that the amygdala is involved in regulating the storage of memory in other brain regions. 相似文献
98.
M Merino J E Peris-Ribera F Torres-Molina A Sánchez-Picó M C García-Carbonell V G Casabó A Martín-Villodre J M Plá-Delfina 《Biopharmaceutics & drug disposition》1989,10(3):279-297
Absorption of the spasmolytic drug baclofen in three selected intestinal segments of living anaesthetized rats in situ, is shown to be a specialized transport mechanism obeying Michaelis-Menten kinetics. Equation parameters were calculated through different procedures, whose features are discussed. A computer method based on the integrated form of Michaelis-Menten equation which reproduces the entire time course of drug absorption from the data found in three intestinal perfusion series at different initial concentrations, yielded Vm and Km values of 12.0 mg h-1 and 8.0 mg, respectively, in the mean segment of the small intestine, a rather selective absorption site for baclofen. Lesser but comparable absorption rates were found in the proximal and distal segments of the small intestine, whereas in colon, drug absorption was negligible. Baclofen transport was significantly reduced in the presence of the enzymatic inhibitor sodium azide. If these results were extrapolated to humans, they would explain the excellent bioavailability profiles reported for baclofen at normal doses in spite of its physicochemical properties, which do not favour passive diffusion. Based on the same principle, the administration of usual doses at shorter time intervals could be recommended, instead of high, when higher plasma levels at steady-state are needed. On the other hand, more than 8-h sustained-release preparations of baclofen should, probably, be avoided. 相似文献
99.
The effects of the GABAB agonist baclofen and the GABAB antagonist CGP 35348, given separately or simultaneously, on the central vestibular system of pigmented rats have been evaluated. Drugs were administered either intramuscularly or intracerebroventricularly. Eye movements were recorded during vestibular, optokinetic and combined visual-vestibular stimulation. Activation of the GABAB receptors by baclofen caused a dose related disturbance of the system, manifested by (1) a decrease of the optokinetic gain, (2) a reduced ability to suppress nystagmus during conflicting vestibular and visual input, and (3) a disability to maintain the eccentric eye position upon a spontaneous saccade. All these effects could be inhibited in a dose-dependent fashion by CGP 35348, suggesting that the findings are specifically related to the GABAB receptor. Given separately, the antagonist did not affect the mentioned parameters. During horizontal acceleratory/deceletory stimulation in darkness baclofen caused a biphasic pattern in the dose-response curves. Small amounts of baclofen caused an increase of the gain and of the duration of poststimulatory nystagmus, while high doses had a depressive action on the same parameters. The stimulating effect of baclofen could be inhibited or even reversed by CGP 35348, which has a depressive effect per se, similar to the effects of baclofen given in the upper range of doses. 相似文献
100.
E. W. Wuis 《Pharmacy World & Science》1987,9(5):249-260
An overview is presented of pathophysiology, classification and measurement of spasticity and of its treatment, especially with dantrolene and baclofen. In spasticity, the balance between excitatory and inhibitory neurotransmitters in the central nervous system is impaired by mechanisms that are for the greater part unknown. Spasticity includes various disorders of motor control, and classification is needed for a meaningful evaluation of antispastic therapy. Cerebral palsy is a specific disorder, sometimes also called spasticity. Measurement of spasticity is complicated and should include signs characteristic of spasticity and parameters for clinical improvement. Dantrolene and baclofen have established their place in the treatment of spastic disorders, but a preference for either drug is hard to give. For tizanidine it is still too early to determine its place in therapy. Dantrolene is a direct acting muscle relaxant which should be avoided in patients with pre-existing liver damage. Its mechanism of metabolism and excretion is for the greater part unknown. The GABA
b
agonist baclofen is a centrally acting muscle relaxant. In patients with impaired renal function the dose should be reduced. Abrupt withdrawal carries the risk of unwanted reactions. TheR(–)-enantiomer has proved to be the active isomer. This means that human trials need reappraisal, especially those relating to the pharmacokinetics of the racemate. 相似文献