Ahrén B, Veith R C, Taborsky G J
Endocrinology. 1987 Jul;121(1):323-31. doi: 10.1210/endo-121-1-323.
We investigated whether pancreatic norepinephrine (NE) infusions could reproduce the inhibition of insulin secretion and the stimulation of glucagon secretion observed during sympathetic nerve stimulation in halothane-anesthetized dogs. Three minutes of stimulating the sympathetic nerves (8 Hz, 1 msec, 10 mA, n = 6) surrounding the pancreatic artery decreased both the blood flow in the superior pancreatic vein (SPV) (delta = -1.7 +/- 0.6 ml/min, P less than 0.05) and the basal pancreatic output of immunoreactive insulin (IRI) (delta = -79 +/- 5%, P less than 0.001). SPV levels of NE increased by 683 +/- 177 pg/ml (P less than 0.02). Infusion of NE into the superior pancreatic artery at the low dose of 12 ng/min (n = 6) reproduced this increase of SPV levels of NE (delta = +740 +/- 130 pg/ml; P less than 0.01) and caused a small reduction of SPV blood flow (delta = -1.0 +/- 0.4 ml/min, P less than 0.05), but did not change pancreatic IRI (delta = -26 +/- 16%, NS). The medium dose of NE (120 ng/min, n = 6) reproduced the nerve stimulation-induced decrease of SPV blood flow (delta = -1.5 +/- 0.2 ml/min; P less than 0.01) and increased the SPV NE levels by 6,306 +/- 1,839 pg/ml (P less than 0.02), yet did not decrease pancreatic IRI output (delta = +62 +/- 49%, NS). The high dose of NE (1,200 ng/min, n = 6) produced an extreme increment of SPV NE levels (delta = +180,000 +/- 44,000 pg/ml, P less than 0.001) and a much larger reduction of SPV blood flow (delta = -3.7 +/- 0.7 ml/min, P less than 0.01) than did nerve stimulation, yet still did not inhibit insulin output (delta = -13 +/- 46%, NS). Ten minutes of sympathetic nerve stimulation increased the pancreatic output of immunoreactive glucagon (IRG) by 1435 +/- 419 pg/min (P less than 0.02). Pancreatic IRG output increased as well during infusion of NE for 10 min at both 12 ng/min (by 575 +/- 205 pg/min, P less than 0.05) and 120 ng/min (by 718 +/- 231 pg/min, P less than 0.05). In marked contrast, during infusion of NE at 1200 ng/min, pancreatic IRG output decreased (by 400 +/- 190 pg/min, P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
我们研究了在氟烷麻醉的犬中，胰腺输注去甲肾上腺素（NE）是否能重现交感神经刺激期间所观察到的胰岛素分泌抑制和胰高血糖素分泌刺激。刺激胰腺动脉周围的交感神经（8赫兹，1毫秒，10毫安，n = 6）三分钟，使胰上静脉（SPV）的血流量（变化量=-1.7±0.6毫升/分钟，P<0.05）和免疫反应性胰岛素（IRI）的基础胰腺分泌量（变化量=-79±5%，P<0.001）均降低。SPV中NE水平升高了683±177皮克/毫升（P<0.02）。以12纳克/分钟的低剂量将NE输注到胰上动脉（n = 6），重现了SPV中NE水平的这种升高（变化量=+740±130皮克/毫升；P<0.01），并使SPV血流量略有减少（变化量=-1.0±0.4毫升/分钟，P<0.05），但未改变胰腺IRI（变化量=-26±16%，无显著性差异）。中等剂量的NE（120纳克/分钟，n = 6）重现了神经刺激引起的SPV血流量减少（变化量=-1.5±0.2毫升/分钟；P<0.01），并使SPV中NE水平升高了6306±1839皮克/毫升（P<0.02），但并未降低胰腺IRI分泌量（变化量=+62±49%，无显著性差异）。高剂量的NE（1200纳克/分钟，n = 6）使SPV中NE水平极度升高（变化量=+180000±44000皮克/毫升，P<0.001），且使SPV血流量的减少幅度比神经刺激时更大（变化量=-3.7±0.7毫升/分钟，P<0.01），但仍未抑制胰岛素分泌（变化量=-13±46%，无显著性差异）。十分钟的交感神经刺激使免疫反应性胰高血糖素（IRG）的胰腺分泌量增加了1435±419皮克/分钟（P<0.02）。在以12纳克/分钟和120纳克/分钟输注NE 10分钟期间，胰腺IRG分泌量也增加（分别增加575±205皮克/分钟，P<0.05和增加718±231皮克/分钟，P<0.05）。与之形成显著对比的是，在以1200纳克/分钟输注NE期间，胰腺IRG分泌量减少（减少400±190皮克/分钟，P<0.05）。（摘要截短于400字）
