Effect of a thrombolytic agent (urokinase) on necrosis after acute myocardial infarction.
Using a two-compartment model with continuous input function, the rate and extent of myocardial damage were calculated from plasma enzyme levels measured in patients suffering from acute myocardial infarction (AMI). Results were compared for four different enzymes. As regards the course of necrosis, two different hypotheses were tested and it was shown that the necrotic process has to be considered as a mulitplicative process rather than as a sudden disintigration of cells due to anoxia. Comparison of results obtained in a group of 5 patients treated with urokianse and in an untreated control group of 10 patients showed that the necrotic phase as defined by the enzyme release from the infarcted area was significantly shortened.
D001219:Aspartate Aminotransferases / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D010450:Endopeptidases / Q000627:therapeutic use*; D005956:Glucose-6-Phosphate Isomerase / Q000378:metabolism; D006801:Humans; D006884:Hydroxybutyrate Dehydrogenase / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008954:Models, Biological; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000201:enzymology; D009206:Myocardium / Q000201:enzymology; D009336:Necrosis / Q000188:drug therapy; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use*
D007770:L-Lactate Dehydrogenase; D006884:Hydroxybutyrate Dehydrogenase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase; D010450:Endopeptidases; D014568:Urokinase-Type Plasminogen Activator; D005956:Glucose-6-Phosphate Isomerase