Studies on intracardiac acid hydrolases in the ischemic myocardial necrosis.
Activities and subcellular distributions of acid hydrolases, cathepsin D, acid phosphatase and beta-glucuronidase in myocardial subfractions were determined serially with reference to the initiation of myocardial necrosis in dog hearts with acute ischemia. The following results were obtained: 1) In the normal myocardium, respectable activities of three enzymes were obtained either in the sarcoplasmic reticulum or in the lysosome-containing fraction. 2) Thirty min after coronary ligation, an increase in the activities was observed in both lysosome and sarcoplasmic reticulum fractions of the ischemic heart muscle. After 60 to 90 min these activities were decreased rapidly in both fractions to about 70% of those of the normal myocardium with an increase in the cytosolic activity. Two to 3 hours after ligation, the reduction in the cytosolic activity was noted, indicating an escape of the enzymes from the necrotic myocardium. The subcellular distribution of these enzymes was further altered in the ischemic heart muscle for 12 to 14 hours reflecting an infiltration of the interstitial cells. These findings suggest that activation and release of acid hydrolases not only in lysosomes but also in the sarcoplasmic reticulum are one of the primary and the earliest factors for the evolution of ischemic myocardial injury which leads to necrosis.
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D002402:Cathepsin D; D002403:Cathepsins / Q000378:metabolism; D003327:Coronary Disease / Q000201:enzymology*; D004285:Dogs; D005966:Glucuronidase / Q000378:metabolism*; D006867:Hydrolases / Q000378:metabolism*; D008247:Lysosomes / Q000201:enzymology; D008929:Mitochondria, Heart / Q000201:enzymology; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D009336:Necrosis
D006867:Hydrolases; D000135:Acid Phosphatase; D005966:Glucuronidase; D002403:Cathepsins; D002402:Cathepsin D