Andersson P O, Holst J, Järhult J
Eur Surg Res. 1979;11(6):409-22. doi: 10.1159/000128091.
Glucose, insulin and glucagon concentrations were determined before, during and after a 60-min period of haemorrhagic hypotension at 60 mm Hg in controls, adrenalectomized and splanchnicectomized cats. Peak increase of arterial plasma glucose concentration in response to haemorrhage was 13.7 +/- 4.3 mM in controls, 10.2 +/- 2.8 mM in adrenalectomized and 3.1 +/- 1.7 mM in splanchnicectomized cats, respectively. Peak portal insulin decrease was 58 +/- 8 and 36 +/- 14 pmol/l in controls and adrenalectomized cats, respectively, whereas insulin levels increased slightly in splanchnicectomized cats during hypovolaemia. Portal plasma glucagon concentration rose by about 250 pmol/l in response to bleeding in all groups of cats. We conclude that the prompt hyperglycaemic and hypoinsulinaemic response to haemorrhage in cats are caused by an adrenergic, 'non-medullary' mechanism, whereas the marked rise in pancreatic glucagon release seems due to factors unrelated to the sympatho-adrenal system.
在对照组、肾上腺切除组和内脏切除组的猫中，测定了60毫米汞柱失血性低血压60分钟期间及前后的葡萄糖、胰岛素和胰高血糖素浓度。对照组猫对出血反应的动脉血浆葡萄糖浓度峰值增加为13.7±4.3毫摩尔/升，肾上腺切除组为10.2±2.8毫摩尔/升，内脏切除组为3.1±1.7毫摩尔/升。对照组和肾上腺切除组猫门静脉胰岛素峰值降低分别为58±8和36±14皮摩尔/升，而内脏切除组猫在低血容量期间胰岛素水平略有升高。所有组的猫出血后门静脉血浆胰高血糖素浓度均升高约250皮摩尔/升。我们得出结论，猫对出血迅速出现的高血糖和低胰岛素反应是由一种肾上腺素能的“非髓质”机制引起的，而胰腺胰高血糖素释放的显著增加似乎是由与交感-肾上腺系统无关的因素导致的。
