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Free access | 10.1172/JCI106252

Studies on the pathogenesis of acute inflammation: IX. The influence of hyperosmolality secondary to hyperglycemia upon the acute inflammatory response induced by thermal injury to ear chambers of rabbits

Sterling K. Ainsworth and Fred Allison Jr.

Department of Medicine, University Medical Center, Jackson, Mississippi 39216

Department of Microbiology, University Medical Center, Jackson, Mississippi 39216

Find articles by Ainsworth, S. in: PubMed | Google Scholar

Department of Medicine, University Medical Center, Jackson, Mississippi 39216

Department of Microbiology, University Medical Center, Jackson, Mississippi 39216

Find articles by Allison, F. in: PubMed | Google Scholar

Published March 1, 1970 - More info

Published in Volume 49, Issue 3 on March 1, 1970
J Clin Invest. 1970;49(3):433–441. https://doi.org/10.1172/JCI106252.
© 1970 The American Society for Clinical Investigation
Published March 1, 1970 - Version history
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Abstract

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.

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