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排序方式: 共有523条查询结果,搜索用时 15 毫秒
91.
Otto L. Wolthuis Herman P. M. van Helden Bert P. C. Melchers Ruud W. Busker Didima M. G. de Groot 《Neuroscience and biobehavioral reviews》1994,18(4):469-486
This mini-review mainly describes a part of the pharmacological research carried out in our laboratory during the past decades, aimed at finding a therapy against intoxication by cholinesterase-inhibiting organophosphates, in particular against the nerve agent soman. In particular soman, because this is one of the nerve agents that consistently appears to be very resistant to treatment. Various experimental approaches are described. Yet, even after all these years of research an adequate (pre)treatment against poisoning by soman is still not available. 相似文献
92.
In rats, the injection of soman (70 μg/kg, SC) resulted in a 90% inhibition of the cholinesterase (ChE) activities in three brain regions. The density (Bmax) for muscarinic acetylcholine receptors (mAChRs) following a single injection of soman was significantly reduced at 2 h after injection in the cortex and hindbrain. Bmax values, however, returned to baseline within 24 h. Subacute (repeated injection every 15 min) treatment with a sublethal dose of soman over 2 h also decreased the density of mAChRs. In both cases the density of mAChRs was reduced by about 15% for the cortex and 17% for the hindbrain (the midbrain was also reduced by 18% for subacute injections). Chronic administration (once daily for 7 days) of soman (20 μg/kg, SC) produced maximal inhibition of ChE activity but did not significantly downregulate mAChRs. Clonidine pretreatment reversed the soman-induced mAChR downregulation in cortex and hindbrain produced by acute soman administration. Thus, marked reduction in the levels of brain ChE is not the only factor involved in the production of mAChR downregulation to cholinesterase inhibitors. 相似文献
93.
西咪替丁对普鲁卡因复合麻醉下琥珀胆碱时—量和阻滞性质的影响 总被引:1,自引:0,他引:1
20例普胸、脊柱外科手术患者,配对分为西咪替了组(1组)和对照组(2组)。 1组麻醉诱导前45分钟肌注西咪替了4mg·kg-1,用加速度仪监测两组患者用普鲁卡因、琥珀胆碱复合液时琥珀胆碱的时-量和阻滞性质的变化,并采血做血清胆碱酯酶活性测定。结果:两组患者静滴流琥珀碱后时-量无显著差异。Ⅰ组转相过程、Ⅱ相阻滞发生时间较2组迟。Ⅰ组诱导时血清胆碱酯酶活性下降33.37%,差异显著。 相似文献
94.
Sowmya Madhavadas 《Nutritional neuroscience》2017,20(9):526-537
Objective: Several dietary supplements are actively being tested for their dual role of alleviating the metabolic perturbations and restricting the consequent cognitive dysfunctions seen in neurodegenerative disorders such as Alzheimer's disease (AD). The aim of the current study was to assess the influence of aqueous extract of cinnamon (CE) on the monosodium glutamate-induced non-transgenic rat model of AD (NTAD) established with insulin resistance, hyperglycaemia, neuronal loss, and cognitive impairment at a very early stage of life.Methods: The experimental design included oral administration of CE (50?mg/kg body weight) for 20 weeks to 2-month and 10-month-old NTAD rats. Following the treatments, the animals attained 7 and 15 months of age, respectively. They were then subjected to behavioural testing, biochemical analysis, and stereology experiments.Results: The results demonstrated that CE treatment improved the insulin sensitivity, increased phosphorylated glycogen synthase kinase-3β (pGSK3β), inhibited the cholinesterase activity, and improved the learning ability in NTAD rats. Histological evaluation has shown an increase in neuron count in the DG sub-field of hippocampus upon treatment with CE.Discussion: These beneficial effects of CE are suggestive of considering cinnamon as a dietary supplement in modulating the metabolic changes and cognitive functions. 相似文献
95.
Summary In mice, Arecoline in vivo dose-dependently increased the cGMP concentrations of the cerebellum and the cerebrum (= parts of cortex, hippocampus, hypothalamus, thalamus, striatum and midbrain) without influencing the cAMP levels. The cholinesterase inhibitors paraoxon and physostigmine caused an elevation only in cerebrum, whereas the cGMP content of the cerebellum even decreased.Pretreatment with atropine prevented the rise in cGMP levels as well as the symptoms of cholinergic stimulation elicited by arecoline or paraoxon. Diazepam reduced cGMP levels below control values and blocked the effect of arecoline, while typical symptoms due to arecoline, e.g., tremor and salivation remained unaffected. The tripeptide prolyl-leucyl-glycinamide (MIF) had no effect on either cGMP values or the peripheral signs of cholinergic stimulation elicited by arecoline.The results show that elevation of cGMP in the central nervous system caused by cholinomimetic agents can be prevented not only by cholinolytics, blocking muscarinic receptors but also by influencing other mechanisms to be discussed. 相似文献
96.
J. L. Willems H. C. De Bisschop A. G. Verstraete C. Declerck Y. Christiaens P. Vanscheeuwyck W. A. Buylaert D. Vogelaers F. Colardyn 《Archives of toxicology》1993,67(2):79-84
We measured in nine patients, poisoned by organophosphorus agents (ethyl parathion, ethyl and methyl parathion, dimethoate, or brompphos), erythrocyte and serum cholinesterase activities, and plasma concentrations of the organophosphorus agent. These patients were treated with pralidoxime methylsulphate (ContrathionR), administered as a bolus injection of 4.42 mg.kg–1 followed by a continuous infusion of 2.14 mg.kg–1/h, a dose regimen calculated to obtain the presumed therapeutic plasma level of 4 mg.l–1, or by a multiple of this infusion rate. Oxime plasma concentrations were also measured. The organophosphorus agent was still detectable in some patients after several days or weeks. In the patients with ethyl and methyl parathion poisoning, enzyme reactivation could be obtained in some at oxime concentrations as low as 2.88 mg.l–1; in others, however, oxime concentrations as high as 14.6 mg.l–1 remained without effect. The therapeutic effect of the oxime seemed to depend on the plasma concentrations of ethyl and methyl parathion, enzyme reactivation being absent as long as these concentrations remained above 30 g.l–1. The bromophos poisoning was rather mild, cholinesterases were moderately inhibited and increased under oxime therapy. The omethoate inhibited enzyme could not be reactivated. 相似文献
97.
György Marosi János Iván László Nagymajtényi Imre Csatlós Anna Tószegi 《Archives of toxicology》1985,57(2):142-143
In anaesthetized guinea-pigs treated with lethal doses of dimethoate, cardiac failure and serious ECG disturbances developed in the early phase of intoxication. The toxic cardiac phenomena appeared to be unrelated to the degree of cholinesterase inhibition, but showed a close correlation with myocardial dimethoate concentration. Cardiac failure and mortality were first observed at a critical pesticide level of about 110 g/g, while a level of 221 g/g resulted in death in all cases. The present investigation refers to the direct effect of the pesticide on the myocardium, independent of its anticholinesterase action. 相似文献
98.
The effects of repeated exposure to a sublethal dose (60 µg/kg; 0.4 LD50) of soman on brain regional acetylcholine (ACh) and choline (Ch) levels, spinal cord cholinesterase (ChE) activity and on water consumption, body weight and gross behavioral changes were examined. Male rats were dosed once a week or three times a week and at 24 h after 2, 4 or 6 weeks of dosing, selected brain tissues and behavior were examined. During the 6-week period, there was no difference between control and soman-dosed rats in water consumption or body weight under either treatment regimen. The animals treated once a week adapted to this exposure regimen well. They exhibited no change in the levels of ACh or Ch in any of the brain areas when examined at the end of 2, 4 or 6 weeks, nor did they show any obvious signs of poisoning. The total ChE activity fluctuated between 70 and 100% of control. When treated three times a week, however, survivors (90%) of the somantreated rats developed signs that progressed in severity to a hyper-reactivity syndrome which consisted of an exaggerated reaction to mild tactile stimuli. Brain ACh levels did not change and ChE activity showed inhibition of 40, 58 and 75% when measured at 2, 4 and 6 weeks, respectively. At the end of 6 weeks, the levels of Ch, except in the striatum, were significantly elevated in brainstem, cerebral cortex, hippocampus, midbrain, and cerebellum (52%, 147%, 68%, 46%, and 91%, respectively), indicating that Ch metabolism in neuronal membranes may be altered following more frequent low-dose soman exposures.The experiments reported here were conducted according to the Guide for Care and Use of Laboratory Animals (1985), as prepared by the Committee on Care and Use of Laboratory Animals, National Research Council, NIH Publication No. 85-23. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense 相似文献
99.
目的 探讨重症肌无力(MG)患者呼吸肌力在中药联合胆碱酯酶抑制剂治疗后的变化.方法 对胆碱酯酶抑制剂耐药的MG患者34例,其中Ⅰ型MG14例,Ⅱ型MG20例.均经溴化吡啶斯的明360~480 mg/d治疗3个月~3年无效复诊,除维持原有治疗外再联合中药饮剂治疗,待临床症状改善时,对溴化吡啶斯的明逐渐减量,继续中药治疗4~6个月.观察治疗前后肺功能:肺活量(VC)、最大自主通气量(MVV)、最大吸气压(PIM)、最大呼气压(PEM)、呼吸中枢驱动压(P0.1)、残气量(RV),分别取实测值占预计值百分比(P0.1除外),并进行临床严重程度评分.结果 34例MG患者经胆碱酯酶抑制剂单独治疗一段时间后,VC、MVV、PIM、PEM、RV等占预计值百分比无明显改善(P均>0.05);联合中药治疗后,MG患者VC、MVV、PIM、PEM占预计值的百分比分别由治疗前的(76.66±18.59)%、(68.03±10.45)%、(43.25±18.16)%、(21.75±14.44)%增加到(86.91±14.87)%、(75.11±11.17)%、(52.66±20.32)%、(28.56±10.06)%,RV由治疗前的(164.94±67.97)%降到(143.16±79.21)%(t值分别为3.41、3.03、3.56、2.36、4.71,P均<0.05);与Ⅱ型MG患者相比,Ⅰ型MG患者PIM[(65.80±28.03)%、(52.66±20.32)%]、PEM[(37.03±20.57)%、(28.56±19.06)%]改善显著(t值分别为3.85、3.16,P均<0.01),另外Ⅱ型MG患者呼吸肌耐力[(108.71±17.56)%]较Ⅰ型MG组[(96.01±14.12)%]改善更加显著(t=3.92,P<0.05).结论 中药联合胆碱酯酶抑制剂能有效地改善对胆碱酯酶抑制剂耐药患者的肺功能和呼吸肌力,与Ⅱ型MG患者相比,Ⅰ型患者肺功能的呼吸肌肌力改善更加明显,但Ⅱ型MG患者呼吸肌耐力的改善优于Ⅰ型MG患者. 相似文献
100.
《Clinical and experimental hypertension (New York, N.Y. : 1993)》2013,35(7-8):697-713
The involvement of an impaired cholinergic neurotransmission in the pathophysiology of cognitive impairment occurring in vascular dementia (VaD), as well as the possibility of treating it by stimulating cholinergic neurotransmission was reviewed. Pre-clinical data suggest that similarly as documented in dementia disorders of neurodegenerative origin, a cholinergic deficit is involved in the pathophysiology of cognitive impairment of vascular origin. In the past, clinical trials have evaluated cholinergic precursors such as lecithin, citicoline and choline alphoscerate. More recent investigations have assessed acetylcholinesterase (AChE) and cholinesterase (ChE) inhibitors such as donepezil, rivastigmine and galantamine.In general, treatment with citicoline, choline alphoscerate, as well as with AChE and ChE inhibitors induced favourable effects on cognitive function in dementia disorders of vascular origin. These positive results should be regarded with caution due to the small number of patients included in controlled clinical trials using cholinergic precursors and to the limited number and sample size of trials with AChE and ChE inhibitors. Among compounds investigated, choline alphoscerate was well tolerated, improved cognitive function in VaD patients to a better extent than citicoline and to similar or better extent than other more recently developed drugs. This particular profile would justify reconsideration of the compound in larger controlled clinical trials for the treatment of cognitive dysfunction associated with dementia disorders of vascular origin. 相似文献