Ainsworth S K, Allison F
J Clin Invest. 1970 Mar;49(3):433-41. doi: 10.1172/JCI106252.
The inflammatory reaction induced in ear chambers of rabbits by heat injury was studied in nondiabetic animals made hyperglycemic with continuous infusions of glucose. Hypertonic solutions of glucose administered intravenously to rabbits induced the following triad: hyperglycemia, hyperosmolality, and metabolic lactic acidosis. It was found that relatively short periods of this metabolic abnormality were associated with a significant reduction in the intensity of the inflammatory reaction. There was no evidence microscopically of circulatory impairment within ear chambers; and since neither arterial hypotension nor oxygen deficit was recorded during experiments, it appeared most likely that decreased leucocytic margination per se best explained the inhibited exudative response. Hyperglycemia seemed the dominant factor responsible for this anti-inflammatory effect. It was found subsequently that hyperglycemia and hyperosmolality without metabolic acidosis impaired cellular exudation just as well.
在通过持续输注葡萄糖使非糖尿病动物血糖升高的情况下,研究了热损伤在兔耳腔中诱导的炎症反应。静脉内给兔注射高渗葡萄糖溶液会引发以下三联征:高血糖、高渗性和代谢性乳酸酸中毒。结果发现,这种代谢异常相对较短的时期与炎症反应强度的显著降低有关。在显微镜下没有证据表明耳腔内存在循环障碍;并且由于实验过程中既未记录到动脉低血压也未记录到氧缺乏,似乎最有可能的是,白细胞贴壁减少本身最能解释渗出反应受到抑制的原因。高血糖似乎是造成这种抗炎作用的主要因素。随后发现,没有代谢性酸中毒的高血糖和高渗性同样会损害细胞渗出。