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48小时葡萄糖输注大鼠胰岛血流增加:中枢和自主神经系统的参与

Increased pancreatic islet blood flow in 48-hour glucose-infused rats: involvement of central and autonomic nervous systems.

作者信息

Atef N, Laury M C, N'Guyen J M, Mokhtar N, Ktorza A, Penicaud L

机构信息

Laboratoire de Physiopathologie de la Nutrition, CNRS URA 307, Université Paris VII, France.

出版信息

Endocrinology. 1997 May;138(5):1836-40. doi: 10.1210/endo.138.5.5094.

DOI:10.1210/endo.138.5.5094
PMID:9112376
Abstract

The pancreatic islet blood flow of rats 24 h after a prolonged (48-h) glucose infusion was investigated using a nonradioactive microsphere technique. In the basal state, islet blood flow was significantly increased in previously hyperglycemic rats (HG) compared to that in controls (C). During an i.v. glucose challenge, both plasma insulin and islet blood flow were increased in the two groups, but these increases were significantly higher in HG than in C rats. Although less pronounced, the results were similar when glucose was injected into the carotid artery toward the brain at a dose that did not modify the peripheral glucose level. The effect of this intracarotid injection was abolished after bilateral subdiaphragmatic vagotomy in both C and HG rats. Furthermore, in the latter group, both plasma insulin concentration and islet blood flow returned to values similar to those observed in the basal state in C rats. After pretreatment with the alpha2-adrenoceptor agonist clonidine, the insulin response to the intracarotid glucose load was totally blunted in the two groups of rats. By contrast, whereas such a pretreatment lowered the glucose-induced increase in islet blood flow in C rats, it was without effect in HG rats. These data suggest that a period of hyperglycemia and/or hyperinsulinemia is sufficient to induce a perturbation of pancreatic islet blood flow, which appears to be mainly due to an increased parasympathetic activity, whereas the decrease in sympathetic tone does not play a role. These modifications in autonomic nervous system activity could be due to alterations in some brain areas involved in "glucose sensing."

摘要

采用非放射性微球技术研究了大鼠长时间(48小时)输注葡萄糖24小时后的胰岛血流情况。在基础状态下,与对照组(C)相比,先前高血糖大鼠(HG)的胰岛血流显著增加。在静脉注射葡萄糖刺激期间,两组的血浆胰岛素和胰岛血流均增加,但HG组的这些增加显著高于C组大鼠。当以不改变外周血糖水平的剂量向大脑方向的颈动脉注射葡萄糖时,尽管不太明显,但结果相似。在C组和HG组大鼠双侧膈下迷走神经切断术后,这种颈动脉注射的效应被消除。此外,在HG组中,血浆胰岛素浓度和胰岛血流均恢复到与C组大鼠基础状态下观察到的值相似。用α2肾上腺素能受体激动剂可乐定预处理后,两组大鼠对颈动脉葡萄糖负荷的胰岛素反应完全被抑制。相比之下,虽然这种预处理降低了C组大鼠葡萄糖诱导的胰岛血流增加,但对HG组大鼠没有影响。这些数据表明,一段高血糖和/或高胰岛素血症足以诱导胰岛血流紊乱,这似乎主要是由于副交感神经活动增加,而交感神经张力降低不起作用。自主神经系统活动的这些改变可能是由于参与“葡萄糖感知”的一些脑区的改变。

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Increased pancreatic islet blood flow in 48-hour glucose-infused rats: involvement of central and autonomic nervous systems.48小时葡萄糖输注大鼠胰岛血流增加:中枢和自主神经系统的参与
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