THE MECHANISM OF VAGAL NERVE-STIMULATION OF GLUCAGON AND INSULIN-SECRETION IN THE DOG
THE MECHANISM OF VAGAL NERVE-STIMULATION OF GLUCAGON AND INSULIN-SECRETION IN THE DOG
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DOI：
10.1210/endo-118-4-1551
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发表时间：
1986-04-01
期刊：
影响因子：
4.8
通讯作者：
TABORSKY, GJ
中科院分区：
文献类型：
--
作者：
AHREN, B;TABORSKY, GJ
在氟烷麻醉的狗上，研究了迷走神经刺激胰高血糖素（IRG）和胰岛素（IRI）分泌的机制。在心脏下方电刺激胸迷走神经的腹侧支和背侧支（10 Hz，5 msec，13.5 mA，10 min）。采集胰十二指肠动脉和上级静脉血浆，测定上级静脉血浆流量，计算IRG和IRI的胰腺净输出量。在迷走神经刺激期间（n = 15），IRG的净胰腺输出加倍（Δ= +0.83 .+-. 0.28 ng/min，P < 0.01;基线= 0.81。0.15 ng/min）和IRI四倍（Δ I）。= +3.5 .+-. 1.5 mU/min，P < 0.025;基线= 1.1 . ±. 0.3 mU/min）。动脉葡萄糖水平增加了7 . ±.从108 ± 2 mg/dl。3 mg/dl（P < 0.005）。阿托品预处理后（n = 7），胰腺IRI对迷走神经刺激的反应为+0.71 . ±-。0.28 mU/min（P < 0.025），下降80%。相比之下，阿托品预处理既不改变IRG反应（Δ IRG），也不改变IRG反应（Δ IRG）。= +0.87 .+-. 0.36 ng/min; P < 0.05）或动脉葡萄糖反应（Δ G）。= +9 .+-. 3 mg/dl; P < 0.025）。六烃铵预处理（n = 9）消除胰腺IRG反应（Δ IRG）。= +0.13 .+-. 0.11 ng/min; NS）、动脉葡萄糖反应（Δ G/min; = +0.5 .+-. 1.9 mg/dl; NS）和胰腺IRI反应（Δ IRI）。= +0.16 .+-. 0.31 mU/min; NS）刺激迷走神经。它的结论是，迷走神经刺激在狗产生一个温和的增加IRG分泌，介导的非毒蕈碱（肽能？）机制，和IRI分泌的显着增加，介导的毒蕈碱机制。这两种反应都依赖于烟碱传递。
The mechanism of vagal nerve stimulation of glucagon (IRG) and insulin (IRI) secretion was investigated in halothane-anesthetized dogs. Both ventral and dorsal branches of the thoracic vagi were stimulated electrically (10 Hz, 5 msec, 13.5 mA, 10 min) below the heart. Arterial and superior pancreaticoduodenal venous plasma were sampled, superior pancreaticoduodenal venous plasma flow was measured, and net pancreatic output of IRG and IRI were calculated. During vagal nerve stimulation (n = 15) net pancreatic output of IRG doubled (.DELTA. = +0.83 .+-. 0.28 ng/min, P < 0.01; baseline = 0.81 .+-. 0.15 ng/min) and IRI quadrupled (.DELTA. = +3.5 .+-. 1.5 mU/min, P < 0.025; baseline = 1.1 .+-. 0.3 mU/min). Arterial glucose levels increased by 7 .+-. 2 mg/dl from 108 .+-. 3 mg/dl (P < 0.005). After atropine pretreatment (n = 7), the pancreatic IRI response to vagal nerve stimulation was +0.71 .+-. 0.28 mU/min (P < 0.025), a reduction of 80%. In contrast, atropine pretreatment changed neither the IRG response (.DELTA. = +0.87 .+-. 0.36 ng/min; P < 0.05) nor the arterial glucose response (.DELTA. = +9 .+-. 3 mg/dl; P < 0.025) to vagal nerve stimulation. Hexamethonium pretreatment (n = 9) abolished the pancreatic IRG response (.DELTA. = +0.13 .+-. 0.11 ng/min; NS), the arterial glucose response (.DELTA. = +0.5 .+-. 1.9 mg/dl; NS) and the pancreatic IRI response (.DELTA. = +0.16 .+-. 0.31 mU/min; NS) to vagal nerve stimulation. It is concluded that vagal nerve stimulation in the dog produces a moderate increase of IRG secretion, mediated by a nonmuscarinic (peptidergic?) mechanism, and a marked increase of IRI secretion, mediated by a muscarinic mechanism. Both responses are dependent on nicotinic transmission.