Bosch M A, García R, Pagani R, Portolés M T, Díaz-Laviada I, Abarca S, Ainaga M J, Risco C, Municio A M
Department of Biochemistry and Molecular Biology I, Faculty of Chemistry, Universidad Complutense, Madrid, Spain.
Br J Exp Pathol. 1988 Dec;69(6):805-12.
Reversible endotoxic shock was induced in adult rats by i.v. injection of Escherichia coli O111:B4 lipopolysaccharide (1.6 mg/100 g). The shock progression was evaluated by measuring serum glucose levels as well as activities of aspartate aminotransferase (GOT) and alkaline phosphatase in serum. A rapid increase of serum glucose levels occurs, after LPS injection, followed by hypoglycaemia (minimum values at 6 h) with progressive reversion to control values. Serum GOT activity increased (twofold) 6 h after endotoxin administration and returned to control values at 72 h. No appreciable changes occurred in serum alkaline phosphatase activity. Endotoxaemia produced a decrease in the cytochrome P-450 levels in all target organs considered: lung, adrenal glands and liver. The progressive decrease in the serum albumin concentration as well as changes of the physical properties of the plasma membranes observed in vivo, can not be explained only by direct interaction of endotoxin with the target organs, underlining the importance of serum mediators in the induction of the shock response.
通过静脉注射大肠杆菌O111:B4脂多糖（1.6毫克/100克）在成年大鼠中诱导出可逆性内毒素休克。通过测量血清葡萄糖水平以及血清中天冬氨酸转氨酶（GOT）和碱性磷酸酶的活性来评估休克进展。注射LPS后血清葡萄糖水平迅速升高，随后出现低血糖（6小时时达到最小值），并逐渐恢复到对照值。内毒素给药6小时后血清GOT活性增加（两倍），并在72小时时恢复到对照值。血清碱性磷酸酶活性未发生明显变化。内毒素血症导致所考虑的所有靶器官（肺、肾上腺和肝脏）中的细胞色素P - 450水平降低。血清白蛋白浓度的逐渐降低以及体内观察到的质膜物理性质的变化，不能仅通过内毒素与靶器官的直接相互作用来解释，这突出了血清介质在休克反应诱导中的重要性。
