Relationship between Serum Concentration and Urinary Output of Trypsin Inhibitor (Hyaluronidase Inhibitor) During Operative Stress

Abstract

The serum concentration and urinary output of trypsin inhibitor was followed in a period before and after operative stress in ten persons. In all subjects the values increased in the postoperative period. No correlation was recorded between the preoperative serum concentrations and urinary trypsin inhibitor outputs, but a highly significant, positive correlation was found between the postoperative increases in serum and urine, demonstrating that the urinary trypsin inhibitor originates from the blood. It is proposed that the urinary trypsin inhibitor is identical with a serum inhibitor which only constitutes a small part of the total trypsin inhibiting activity in serum in the normal state, but whose concentration is markedly increased during stress. The observations could be explained by a passive excretion of the substance in the kidneys, i.e. a glomerular filtration without tubular secretion or reabsorption. The clearance of the compound is estimated to be 0.08 ml per minute (average, for ten persons) but with large individual variations (from 0.02 to 0.12 ml/min) suggesting individual variation in the glomerular permeability to the substance.

Beneficial Effects of the Urinary Trypsin Inhibitor Urinastatin on Renal Insults Induced by Gentamicin and Mercuric Chloride (HgCl₂) Poisoning

“…It inhibits the enzymatic activities of a-chymotrypsin, leukocyte elastase, hyaluronidase, etc., in addition to those of trypsin, in multiple ways [28,29]. The physiological role of urinastatin is not clear, but presumably plays some preventive role against invasion, because its urinary excretion in creases during infection, pyrexia, cancer, pregnancy, shock, surgery, and administration of glucocorticoid [30,31] and because the increase in its urinary excretion is closely associated with the increase in the blood glucocorticoid level [32].…”

Rapid Accumulation of Plasma Acid-Stable Trypsin Inhibitor in Experimental Acute Renal Injury

“…These findings sug gest that ASTI was being produced in the blood or released into it almost constantly. ASTI activity in the sham-operated group was also elevated at 24 h. In 1961, Faarvang and Lauritsen [17] reported an elevation of UTI activity following surgical operations. It was assumed that the elevation of UTI activ ity was due to an elevation of blood ASTI activity which has been proposed to repre sent one origin of UTI.…”