Stone J P, Schutzer S F, McCoy S, Drucker W R
Am Surg. 1977 Jan;43(1):1-5.
Normal rats subjected to hypovolemic shock (Wiggers model) exhibited the characteristic rise in blood glucose as well as the initial fall in hematocrit indicative of plasma refill. Concurrently there was a rise in osmolality. Late in shock these animals became hypoglycemic and the hematocrit rose despite a persisting hyperosmolality. Rats which had been deprived of food for 24 hours in order to deplete the liver glycogen did not become hyperglycemic after hemorrhage and had a less marked fall in hematocrit. The plasma osmolality rose to the same high level as that of the fed rats but the rise was slower. From this we conclude that glucose may be largely responsibile for the rise in osmolality early in shock in fed animals but it is not responsible for the continuing hyperosmolality in fed or fasted animals. Nor is it responsible for the initial rise in fasted animals. Hyperosmolality may delay but does not prevent fluid loss from the capillaries late in shock.
遭受低血容量性休克（维格斯模型）的正常大鼠表现出血糖特征性升高以及血细胞比容最初下降，这表明血浆得到补充。同时，渗透压升高。休克后期，这些动物出现低血糖，尽管渗透压持续升高，但血细胞比容仍升高。为耗尽肝糖原而禁食24小时的大鼠在出血后未出现高血糖，血细胞比容下降也不明显。血浆渗透压升至与喂食大鼠相同的高水平，但升高速度较慢。由此我们得出结论，葡萄糖可能在很大程度上导致喂食动物休克早期渗透压升高，但它并非导致喂食或禁食动物持续高渗的原因。它也不是禁食动物最初渗透压升高的原因。高渗可能会延迟但不会阻止休克后期毛细血管中的液体流失。
