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大鼠亚急性给予氨、硫醇和短链脂肪酸后,脑内苯二氮䓬受体增加。

An increase in cerebral benzodiazepine receptors induced by a subacute administration of ammonia, mercaptans and short-chain fatty acids in rats.

作者信息

Baraldi M, Zeneroli M L, Ventura E, Vezzelli C

机构信息

Department of Pharmaceutical Sciences, Modena University, Italy.

出版信息

Clin Sci (Lond). 1987 Dec;73(6):669-71. doi: 10.1042/cs0730669.

DOI:10.1042/cs0730669
PMID:2826071
Abstract
  1. In the search to identify peripheral toxins which could be responsible for the supersensitivity of brain benzodiazepine receptors in experimental models of hepatic encephalopathy, [3H]diazepam-binding studies have been performed on brain tissues of normal rats treated with ammonium chloride, dimethyldisulphide and octanoic acid administered alone or in combination. 2. The subacute administration of the three toxins in combination induced a 30% increase in the number of benzodiazepine recognition sites. The administration of these toxins alone or in combination showed that this increase was mainly linked to the synergistic action of dimethyldisulphide or octanoic acid with ammonia, since dimethyldisulphide plus octanoic acid was ineffective. 3. These observations seem to reinforce the suggestion that these three toxins are able to induce neurochemical derangements similar to those described in experimental hepatic encephalopathy.
摘要
  1. 在寻找可能导致肝性脑病实验模型中脑苯二氮䓬受体超敏的外周毒素的过程中,对单独或联合给予氯化铵、二甲基二硫和辛酸的正常大鼠脑组织进行了[3H]地西泮结合研究。2. 三种毒素联合亚急性给药导致苯二氮䓬识别位点数量增加30%。单独或联合给予这些毒素表明,这种增加主要与二甲基二硫或辛酸与氨的协同作用有关,因为二甲基二硫加辛酸无效。3. 这些观察结果似乎支持了这样的观点,即这三种毒素能够诱发与实验性肝性脑病中所描述的类似的神经化学紊乱。

相似文献

1
An increase in cerebral benzodiazepine receptors induced by a subacute administration of ammonia, mercaptans and short-chain fatty acids in rats.大鼠亚急性给予氨、硫醇和短链脂肪酸后,脑内苯二氮䓬受体增加。
Clin Sci (Lond). 1987 Dec;73(6):669-71. doi: 10.1042/cs0730669.
2
Toxins in hepatic encephalopathy: the role of the synergistic effect of ammonia, mercaptans and short chain fatty acids.
Arch Toxicol Suppl. 1984;7:103-5. doi: 10.1007/978-3-642-69132-4_12.
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Visual evoked potentials in encephalopathy induced by galactosamine, ammonia, dimethyldisulfide, and octanoic acid.
Hepatology. 1982 Sep-Oct;2(5):532-8. doi: 10.1002/hep.1840020504.
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Effect of ammonium chloride on the astrocyte benzodiazepine receptor.氯化铵对星形胶质细胞苯二氮䓬受体的影响。
Brain Res. 1989 Jul 31;493(2):362-5. doi: 10.1016/0006-8993(89)91171-2.
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Hepatic encephalopathy. Application of visual evoked responses to test hypotheses of its pathogenesis in rats.肝性脑病。视觉诱发电位在大鼠肝性脑病发病机制假说检验中的应用。
J Hepatol. 1987 Feb;4(1):118-26. doi: 10.1016/s0168-8278(87)80018-1.
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Hepatic encephalopathy. Experimental studies in a rat model of fulminant hepatic failure.肝性脑病。暴发性肝衰竭大鼠模型的实验研究。
J Hepatol. 1985;1(3):301-11. doi: 10.1016/s0168-8278(85)80057-x.
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[3H]Ro 15-1788 binding to benzodiazepine receptors in mouse brain in vivo: marked enhancement by GABA agonists and other CNS drugs.[3H]Ro 15 - 1788在体内与小鼠脑内苯二氮䓬受体的结合:GABA激动剂和其他中枢神经系统药物的显著增强作用
Eur J Pharmacol. 1987 Oct 27;142(3):373-84. doi: 10.1016/0014-2999(87)90076-8.
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Regional GABA/benzodiazepine receptor/chloride channel coupling after acute and chronic benzodiazepine treatment.急性和慢性苯二氮䓬治疗后的局部γ-氨基丁酸/苯二氮䓬受体/氯离子通道偶联
Eur J Pharmacol. 1989 Aug 11;167(1):57-65. doi: 10.1016/0014-2999(89)90747-4.
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Effect of phenol and sodium octanoate on the astrocyte benzodiazepine receptor.苯酚和辛酸钠对星形胶质细胞苯二氮䓬受体的影响。
Brain Res. 1990 Apr 30;514(2):349-51. doi: 10.1016/0006-8993(90)91431-f.
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Effect of hepatic failure toxins on regenerative enzymes in the liver after injury with galactosamine in the rat.
J Lab Clin Med. 1989 Apr;113(4):463-8.

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