Ware J, Ljungqvist O, Norberg K A, Nylander G
Acta Chir Scand. 1982;148(8):641-6.
Fed and 24-30 hour starved rats were submitted to haemorrhagic hypotension, 70 mmHg, with a modified Wigger's system. Neuroleptanalgesia was used to ensure a normal degree of stress reactivity. Despite fed animals losing 53% of their original blood volume (BV) and starved animals 47% (BV = 6% prestarved body weight), blood gas data and creatinine levels confirmed a well intact and compensated status in both groups. Fed animals compensated for the greater haemorrhage with a haematocrit reduction which was double that in starved animals. When the alterations in osmole skeletons were compared, evidence for an intracellular fluid (ICF) shift to the interstitium was obtained in fed rats. Their NaCl space increased by 5.5%. Glucose increased its osmolar effect by 224% among fed animals and was reduced in those which had been starved. Glucose was identified as the solute causing an acute mobilisation of ICF to the interstitium.
将喂食后的大鼠和饥饿24 - 30小时的大鼠通过改良的维格斯系统使其处于70毫米汞柱的出血性低血压状态。使用神经安定镇痛法以确保应激反应程度正常。尽管喂食后的动物失血达其原始血容量（BV）的53%，饥饿的动物失血达47%（BV = 饥饿前体重的6%），但两组的血气数据和肌酐水平均证实其状态良好且处于代偿状态。喂食后的动物通过降低血细胞比容来代偿更大程度的出血，其降低幅度是饥饿动物的两倍。当比较渗透骨架的变化时，发现喂食后的大鼠存在细胞内液（ICF）向间质转移的证据。它们的氯化钠间隙增加了5.5%。在喂食后的动物中，葡萄糖的渗透作用增加了224%，而在饥饿的动物中则降低。葡萄糖被确定为导致ICF急性向间质转移的溶质。
