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肝脏葡萄糖感受器在犬深度低血糖诱导的整合交感神经反应中的作用。

The role of liver glucosensors in the integrated sympathetic response induced by deep hypoglycemia in dogs.

作者信息

Hamilton-Wessler M, Bergman R N, Halter J B, Watanabe R M, Donovan C M

机构信息

Department of Physiology, University of Southern California, Los Angeles 90033.

出版信息

Diabetes. 1994 Aug;43(8):1052-60. doi: 10.2337/diab.43.8.1052.

Abstract

The significance of the portohepatic glucosensors for counterregulation in deep hypoglycemia (i.e., glycemia < 2.8 mM) was studied in chronically cannulated male mongrel dogs in the conscious state. A total of 16 experiments were carried out on 6 dogs using the liver clamp technique under hyperinsulinemic conditions (insulin infusion, 39 pmol.min-1.kg-1, 0-150 min). The level of glycemia presented to the liver was made to differ from the systemic arterial glucose level via portal glucose infusion. Tracer-determined rates of glucose clearance and hepatic glucose output (HGO) were assessed using D-[3-3H]glucose (0.26 microCi.min-1). Three protocols were used. In protocol I, liver clamp, systemic hypoglycemia at 2.60 +/- 0.09 mM, and liver glycemia at 3.86 +/- 0.05 mM were achieved with portal glucose infusion (28.2 +/- 3.0 mumol.min-1.kg-1). For protocol II, glucose was infused peripherally (18.2 +/- 4.3 mumol.min-1.kg-1), while systemic and liver glycemia were sustained at deep hypoglycemia, 2.50 +/- 0.08 mM. In protocol III, via peripheral glucose infusion (62.9 +/- 5.8 mumol.min-1.kg-1), systemic and liver glycemia were maintained at a level matched to the liver glycemia during protocol I (3.98 +/- 0.05 mM, P > 0.10). When compared with protocols I and III, the catecholamine response above basal was significantly greater during protocol II with liver and systemic deep hypoglycemia (7.30 +/- 1.51 and 2.89 +/- 0.5 nM for epinephrine and norepinephrine, respectively, P < 0.005). These values reflect net increases in the catecholamine responses of 100% and 85% for epinephrine and norepinephrine when compared with protocol I.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在清醒状态下,对慢性插管的雄性杂种犬研究了门静脉-肝脏葡萄糖感受器在深度低血糖(即血糖<2.8 mM)时对抗调节的意义。在6只犬身上共进行了16次实验,采用肝脏钳夹技术,处于高胰岛素血症状态(胰岛素输注,39 pmol·min⁻¹·kg⁻¹,0 - 150分钟)。通过门静脉输注葡萄糖,使肝脏所接触的血糖水平与体循环动脉血糖水平不同。使用D-[3-³H]葡萄糖(0.26微居里·min⁻¹)评估示踪剂测定的葡萄糖清除率和肝脏葡萄糖输出(HGO)。采用了三种方案。在方案I中,通过门静脉输注葡萄糖(28.2±3.0 μmol·min⁻¹·kg⁻¹),实现肝脏钳夹、全身低血糖至2.60±0.09 mM以及肝脏血糖至3.86±0.05 mM。在方案II中,外周输注葡萄糖(18.2±4.3 μmol·min⁻¹·kg⁻¹),同时全身和肝脏血糖维持在深度低血糖水平,即2.50±0.08 mM。在方案III中,通过外周输注葡萄糖(62.9±5.8 μmol·min⁻¹·kg⁻¹),全身和肝脏血糖维持在与方案I期间肝脏血糖相匹配的水平(3.98±0.05 mM,P>;0.10)。与方案I和III相比,在方案II肝脏和全身深度低血糖期间,基础水平以上的儿茶酚胺反应显著更大(肾上腺素和去甲肾上腺素分别为7.30±1.51和2.89±0.5 nM,P<;0.005)。与方案I相比,这些值反映肾上腺素和去甲肾上腺素的儿茶酚胺反应净增加了100%和85%。(摘要截断于250字)

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