Histaminergic contribution to the metabolic effects of neuroglucopenia.
Histaminergic contribution to the metabolic effects of neuroglucopenia.
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组胺能对神经血糖减少症的代谢作用的贡献。
DOI：
10.1152/ajpregu.1997.272.6.r1918
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Abumrad,NN
中科院分区：
文献类型：
--
作者：
Molina,PE;Williams,P;Abumrad,NN
我们研究了中枢组胺受体(H1和H2)阻断在清醒犬脑室内2-脱氧-D-葡萄糖(2-DG)葡萄糖调节反应中的作用。脑室注射2-DG(2.5 mg·kg~(-1)·min~(-1)，15分钟)可使血糖(2倍)、血乳酸(4倍)和甘油(2倍)水平升高。用同位素测定的肝脏葡萄糖生成率(Ra)增加了两倍。血浆肾上腺素、去甲肾上腺素、胰岛素、胰高血糖素和皮质醇水平也显著高于基础水平。2-DG前15分钟脑室注射赛庚啶和西咪替丁(各100微克)可使2-DG诱导的高血糖降低约50%，并延缓和减弱2-DG诱导的血糖Ra升高(约85%比1组的2倍)。使用H1和H2拮抗剂可抑制肾上腺素、去甲肾上腺素和高血糖素对神经性糖减少的反应，但不影响皮质醇反应。这些发现表明，神经性糖减少症的一些代谢效应，特别是高血糖反应、肝脏对糖异生前体的摄取增加以及葡萄糖Ra的增加，部分是通过中枢组胺能受体激活来调节的。这似乎是通过组胺能激活对中枢神经糖减少症的自主神经和激素反应的影响而实现的。
We examined the contribution of central histamine receptor (H1 and H2) blockade to the glucoregulatory responses to intracerebroventricular 2-deoxy-D-glucose (2-DG) in conscious dogs. Intracerebroventricular 2-DG (2.5 mg.kg-1.min-1 for 15 min) increased plasma glucose (2-fold), blood lactate (4-fold), and glycerol (2-fold) levels. The rate of hepatic glucose production (Ra), determined isotopically, was increased two-fold. Significant increases over basal were also noted in plasma epinephrine, norepinephrine, insulin, glucagon, and cortisol. Pretreatment with cyproheptadine and cimetidine (100 micrograms each icv 15 min before 2-DG) attenuated the 2-DG-induced hyperglycemia by approximately 50% and delayed and attenuated the increase in glucose Ra (approximately 85% vs. 2-fold in group 1). Pretreatment with H1 and H2 antagonists inhibited the increases in epinephrine, norepinephrine, and glucagon in response to neuroglucopenia but did not affect the cortisol response. These findings suggest that some of the metabolic effects of neuroglucopenia, particularly the hyperglycemic response, the increased hepatic uptake of gluconeogenic precursors, and the enhanced glucose Ra, are partly mediated through central histaminergic receptor activation. This appears to be through effects of histaminergic activation on the autonomic and hormonal responses to central neuroglucopenia.