White G L, Archer L T, Beller B K, Holmes D D, Hinshaw L B
Circ Shock. 1977;4(3):231-9.
This laboratory has documented a progressively developing hypoglycemia associated with systemic hypotension, hepatosplanchnic pathology, and death in endotoxin-shocked dogs. Recent data documented accelerated uptake of glucose in blood following endotoxin, with certain components of the buffy coat responsible for the increased uptake. The present study utilizing the awake dog assayed a possible protective role of leukocytes against the lethal effects of endotoxin. Animals were divided into paired groups: saline controls (Group I) and endotoxin experimentals (Group II). Group II animals were injected intravenously with sublethal doses of E. coli endotoxin on 2 successive days (Days 1 and 2), LD100 on the third day, and 2 X LD100 on Day 4. The control group received equal volumes of saline on Days 1, 2, and 3, but on Day 4 received a superlethal dose of endotoxin identical to the experimental group. The awake dog became febrile and exhibited initial leukopenia with subsequent marked leukocytosis in response to endotoxin. Lethal hypoglycemia was not seen in animals demonstrating initial leukocytosis (zero time) on the day of superlethal endotoxin challenge, while animals with initial normal leukocyte counts died with low glucose concentrations (mean, 40 mg%). Results suggest that an initial leukocytosis and sustained gluconeogenic function are important factors in survivability to endotoxin shock.
本实验室已记录到内毒素休克犬出现与全身性低血压、肝脾病理改变及死亡相关的进行性低血糖。近期数据表明，内毒素作用后血液中葡萄糖摄取加速，其中血沉棕黄层的某些成分导致了摄取增加。本研究利用清醒犬测定了白细胞对内毒素致死效应的可能保护作用。动物被分为配对组：生理盐水对照组（I组）和内毒素实验组（II组）。II组动物连续2天（第1天和第2天）静脉注射亚致死剂量的大肠杆菌内毒素，第3天注射致死剂量（LD100），第4天注射2倍LD100剂量。对照组在第1、2和3天接受等量生理盐水，但在第4天接受与实验组相同的超致死剂量内毒素。清醒犬对内毒素产生发热反应，最初出现白细胞减少，随后白细胞显著增多。在超致死剂量内毒素攻击当天表现出最初白细胞增多（零时）的动物未出现致死性低血糖，而最初白细胞计数正常的动物死于低血糖浓度（平均40mg%）。结果表明，最初的白细胞增多和持续的糖异生功能是内毒素休克存活的重要因素。
