Naylor J M, Kronfeld D S
Am J Physiol. 1985 Mar;248(3 Pt 1):E309-16. doi: 10.1152/ajpendo.1985.248.3.E309.
Sheep were prepared with catheters in an artery and mesenteric, portal, and hepatic veins. Blood flows and metabolite concentration differences were measured across liver and gut. Net organ production rates were calculated for liver, portal drained viscera, and extrasplanchnic regions. Arterial glucose concentration rose for 2 h after endotoxin administration. The hyperglycemia was associated with increased hepatic glucose production. Hypoglycemia developed between 3 and 8 h when hepatic glucose production decreased closer to control values. Arterial glucagon concentrations rose to high levels during the hypoglycemic period. Neither hepatic blood flow or oxygen delivery limited glucose production; uptake of the gluconeogenic substrate lactate was reduced on some occasions. Glucose utilization was increased in shock. Portal glucose utilization accounted for 14.5% of nonhepatic glucose utilization. Increased portal glucose utilization was not related to plasma insulin concentrations or insufficient oxygen supply to the gut. Hyperglycemia drove glucose utilization. Although plasma insulin concentrations rose significantly in endotoxemia, the increase in pancreatic insulin output was much smaller and failed to attain statistical significance.
给绵羊在动脉、肠系膜静脉、门静脉和肝静脉中插入导管。测量肝脏和肠道的血流及代谢物浓度差异。计算肝脏、门静脉引流内脏和内脏外区域的净器官产生率。内毒素给药后2小时动脉葡萄糖浓度升高。高血糖与肝脏葡萄糖生成增加有关。在3至8小时之间出现低血糖，此时肝脏葡萄糖生成降至接近对照值。低血糖期间动脉胰高血糖素浓度升至高水平。肝脏血流和氧输送均未限制葡萄糖生成；某些情况下糖异生底物乳酸的摄取减少。休克时葡萄糖利用率增加。门静脉葡萄糖利用率占非肝脏葡萄糖利用率的14.5%。门静脉葡萄糖利用率增加与血浆胰岛素浓度或肠道氧供应不足无关。高血糖驱动葡萄糖利用。虽然内毒素血症时血浆胰岛素浓度显著升高，但胰腺胰岛素分泌的增加幅度小得多，且未达到统计学显著性。
