Abstract
Acute inflammation was induced by injecting carrageenan into a 6 day old air pouch in mice. Sodium aurothiomalate was then given twice to each of three groups of mice via different routes. It was found that the mice injected intravenously with sodium aurothiomalate showed the most striking reduction in the number of exudate leucocytes in the inflammatory cavity, although the amount of gold found in their inflamed pouch lining tissue was the least. The amount of gold in plasma was highest in the mice injected intravenously with sodium aurothiomalate and the least amount of gold was found in the mice injected directly into the air pouch with sodium aurothiomalate. The amount of gold in the inflamed pouch lining tissue reached its peak at 24 hours after injection and a significant decrease of exudate leucocytes was only seen 24 and 72 hours after injection. The amount of gold in the exudate fluid was negligible at all the times studied. No significant difference was noted in the degree of inflammatory suppression when increasing doses of sodium aurothiomalate were injected into the air pouch. These findings show that there is no direct correlation between the gold concentration in the inflamed tissue and suppression of the inflammatory reactions in the cavity. Chemotactic and phagocytic analysis of leucocytes in the exudate showed that there was a significant suppression of the neutrophil activities in all the mice treated with sodium aurothiomalate. It is therefore concluded that the significant reduction in the number of exudate leucocytes at the carrageenan induced inflammatory site after treatment with sodium aurothiomalate is most likely due to the direct action of gold on the functional activities of circulating neutrophils.
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