THE CHEMISTRY OF LOCAL DERMAL INFLAMMATION

[摘要] Inflammation produced 2 major chemical changes in the dermis of rats, one local to and the other distant from the site of injury. Locally, there was a decrease in dermal collagen which was more pronounced after eschar formation. Associated with this loss was a marked local increase in dermal hexosamine and a non-collagenous protein. Evidence for the dermal origin of glycoproteins in the necrotic lesion was presented. During inflammation, the total lipid concentration of the skin decreased, while the water content of the necrotic tissue increased from 55 to 65% of the tissue weight. After eschar formation, the water content fell to 60% of the tissue weight. Subsequent to eschar formation, and during the period of maximum local collagen loss, there was a significant increase in circulating hydroxyproline. Distant from the site of local injury, there was an immediate decrease in both 0.5 [image] saline soluble and insoluble collagen. This loss in insoluble collagen was compensated for with respect to total dermal nitrogen concentration, which did not change, by an increase in insoluble non-collagenous protein. Associated with these changes in the insoluble dermal components was an increase in citrate soluble collagen. The specificity of this loss in dermal collagen with local inflammation suggested the action of a dermal collagenase. Previous work on the effects of cortisol and Dilantin upon the chemistry of rat skin suggested strongly that the specific decrease in the dermal collagen content of uninjured skin distant from the site of local inflammation was a composite of 2 processes: (1) the enzymatic degradation of insoluble collagen and (2) the attempted synthesis of new collagen to replace that being removed by this collagenase activity.