Siaud P, Mekaouche M, Givalois L, Balmefrezol M, Marcilhac A, Ixart G
Laboratory of Experimental Neuroendocrinology, Faculty of Medicine, INSERM U 297, Marseille, France.
Physiol Res. 1995;44(4):227-31.
Previous morphological and physiological studies have suggested that the adrenergic innervation of the dorsal motor nucleus of the vagus nerve (dmnX) is involved in direct synaptic inhibition of parasympathetic preganglionic neurones of the vagus that control secretion of pancreatic insulin. We investigated the effects of bilateral 6-hydroxydopamine (6-OHDA) lesions of adrenergic innervation of the dmnX on pancreatic insulin secretion and glycaemia in normal and vagotomized rats. After two weeks the 6-OHDA lesions produced a marked increase in circulating insulin levels, but no change in glycaemia. Hyperinsulinaemia after adrenergic denervation of the dmnX was more pronounced when a glucose bolus was injected intraarterially. Bilateral subdiaphragmatic vagotomy reversed the observed hyperinsulinaemia. This targeted pharmacological lesion of the adrenergic innervation of dmnX thus causes hypersecretion by pancreatic B cells, an effect which requires an intact vagus nerve.
以往的形态学和生理学研究表明，迷走神经背运动核（dmnX）的肾上腺素能神经支配参与了对控制胰腺胰岛素分泌的迷走神经副交感神经节前神经元的直接突触抑制。我们研究了dmnX肾上腺素能神经支配的双侧6-羟基多巴胺（6-OHDA）损伤对正常大鼠和迷走神经切断大鼠胰腺胰岛素分泌和血糖的影响。两周后，6-OHDA损伤使循环胰岛素水平显著升高，但血糖无变化。当动脉内注射葡萄糖推注时，dmnX肾上腺素能去神经后的高胰岛素血症更为明显。双侧膈下迷走神经切断术可逆转观察到的高胰岛素血症。因此，这种针对dmnX肾上腺素能神经支配的药理学损伤导致胰腺B细胞分泌过多，这种效应需要完整的迷走神经。
