Havel P J, Mundinger T O, Taborsky G J
Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis 95616, USA.
Am J Physiol. 1996 Jan;270(1 Pt 1):E20-6. doi: 10.1152/ajpendo.1996.270.1.E20.
To determine if pancreatic sympathetic nerves can contribute to increased glucagon secretion during hypoglycemia, plasma glucagon and pancreatic glucagon secretion in situ were measured before and during insulin-induced hypoglycemia in three groups of halothane-anesthetized dogs. All dogs were bilaterally vagotomized to eliminate the input from pancreatic parasympathetic nerves. One group of dogs received only vagotomy (VAGX). A second group was vagotomized and adrenalectomized (VAGX + ADX). A third group received vagotomy, adrenalectomy, plus surgical denervation of the pancreas (VAGX + ADX + NERVX) to prevent activation of pancreatic sympathetic nerves. In dogs with VAGX only, hypoglycemia increased plasma epinephrine (Epi), pancreatic norepinephrine (NE) output (+320 +/- 140 pg/min, P < 0.05), arterial plasma glucagon (+28 +/- 12 pg/ml, P < 0.01), and pancreatic glucagon output (+1,470 +/- 370 pg/min, P < 0.01). The addition of ADX eliminated the increase of Epi but did not increase pancreatic NE output (+370 +/- 190 pg/min, P < 0.025), arterial plasma glucagon (+20 +/- 5 pg/ml, P < 0.01), or pancreatic glucagon output (+810 +/- 200 pg/min, P < 0.01). In contrast, the addition of pancreatic denervation eliminated the increase of pancreatic NE output (-20 +/- 40 pg/min, P < 0.05 vs. VAGX), the arterial glucagon (+1 +/- 2 pg/ml, P < 0.01 vs. VAGX), and pancreatic glucagon output responses (+210 +/- 280 pg/min, P < 0.025 vs. VAGX) to hypoglycemia. Thus activation of pancreatic sympathetic nerves can contribute to the increased glucagon secretion during severe insulin-induced hypoglycemia in dogs.
为了确定胰腺交感神经是否会在低血糖期间促使胰高血糖素分泌增加，在三组氟烷麻醉的犬中，于胰岛素诱导的低血糖之前及期间，测定了血浆胰高血糖素及胰腺原位胰高血糖素分泌情况。所有犬均行双侧迷走神经切断术以消除胰腺副交感神经的传入。一组犬仅接受迷走神经切断术（VAGX）。第二组犬行迷走神经切断术及肾上腺切除术（VAGX + ADX）。第三组犬接受迷走神经切断术、肾上腺切除术及胰腺手术去神经支配（VAGX + ADX + NERVX）以防止胰腺交感神经激活。在仅行VAGX的犬中，低血糖使血浆肾上腺素（Epi）、胰腺去甲肾上腺素（NE）输出增加（+320±140 pg/min，P < 0.05）、动脉血浆胰高血糖素增加（+28±12 pg/ml，P < 0.01）以及胰腺胰高血糖素输出增加（+1470±370 pg/min，P < 0.01）。肾上腺切除术消除了Epi的增加，但未增加胰腺NE输出（+370±190 pg/min，P < 0.025）、动脉血浆胰高血糖素（+20±5 pg/ml，P < 0.01）或胰腺胰高血糖素输出（+810±200 pg/min，P < 0.01）。相反，胰腺去神经支配消除了胰腺NE输出的增加（-20±40 pg/min，与VAGX相比P < 0.05）、动脉胰高血糖素（+1±2 pg/ml，与VAGX相比P < 0.01）以及胰腺胰高血糖素输出对低血糖的反应（+210±280 pg/min，与VAGX相比P < 0.025）。因此，胰腺交感神经激活可促使犬在严重胰岛素诱导的低血糖期间胰高血糖素分泌增加。
