Abstract
A useful model of inflammation which approximates rheumatoid arthritis in man is adjuvant induced polyarthritis in the rat. This debilitating systemic disease, first described by Stoerck (1) and by Pearson (2) is provoked by a single injection of a mixture composed of heat killed mycobacteria in liquid paraffin. In addition to the pathologic changes of the skeletal and connective tissues, it is well documented that rats with adjuvant disease also suffer aberrant liver function. Included are decreased glycogen storage (3), derangement in various enzymic capacities to metabolize drugs (4, 5), decreased albumin-mercaptalbumin synthesis (6-8), and enhanced synthesis of alpha-macroglobu-lins and fibrinogen (9).
Since it is generally held that the liver is an important regulatory organ for serum amylase, we thought it would be of interest to study the effect of adjuvant disease on this enzyme.
Materials and Methods. Male Charles River, Lewis strain rats weighing 150 g at the start were used. Heat killed mycobac-terial cells (Difco) in light mineral oil were injected into the subplantar area of the hind-paw. At appropriate times thereafter cardiac blood was withdrawn, allowed to clot, and the serum harvested. In some instances urine samples were also taken. Amylase activity was assayed immediately. Each sample was diluted 50-fold in sodium phosphate buffer, 0.02 M, pH 7.0, with 0.005 M sodium chloride. To a 0.2 ml aliquot of each diluted sample was added 1.0 ml of dyed soluble starch substrate (DyAmyl-L Warner-Lambert Co.). After 10 min at 37° unhydrolyzed starch was precipitated with 5 ml of DyAmyl precipitant solution. Following centrifugation the supernatant was decanted and its optical density at 540 nm minus the optical density of an identical sample precipitated at zero time was taken as a measure of amylase activity.
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