Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

N-acetyl-beta-glucosaminidase (EC 3.2.1.30, recommended name beta-N-Acetylglucosaminidase) was found to be a constituent of human cardiac lysosomes. beta-glucuronidase was also found in this tissue, while lysozyme, an enzyme present in leucocyte lysosomes, was not detectable in the heart. The activities of both N-acetyl-beta-glucosaminidase and beta-glucuronidase were elevated in plasma during the first 24 h after the onset of chest pain in patients with acute myocardial infarction and the peak levels of N-acetyl-beta-glucosaminidase correlated well with those of creatine kinase. N-acetyl-beta-glucosaminidase showed a further rise in plasma activity which gave a peak at 72 h after the onset of chest pain and this was accompanied by a rise in lysozyme activity. It is suggested that lysosome disruption caused by myocardial cell necrosis was responsible for the initial rise in plasma lysosomal enzyme activity and that the subsequent inflammatory reaction gave rise to the second peak.
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PMID:Plasma lysosomal enzyme activity in acute myocardial infarction. 64 16

The activity of N-acetyl-beta-glucosaminidase (NAG) was found to be increased in serial plasma samples from patients with acute myocardial infarction (AMI). Maximum activity occurred 18 hr after the onset of chest pain, and a further peak of activity was found at 72 hr. Four isozymes of NAG were resolved from samples of human myocardium. All four isozymes were present in plasma from patients with AMI but not in normal plasma. beta-Glucuronidase, which is also present in myocardium, had increased activity in plasma at 18 hr but not at 72 hr in patients with AMI. Lysozyme, a lysosomal enzyme in white blood cells, had increased activity in plasma at 72 hr. There was a linear relationship (r = 0.98) between peak levels of NAG at 18 hr and the peak activity of the MB-isozyme of creatine kinase (CK-MB). Three groups of 10 patients were treated with drugs known to stabilize lysosomes during experimental myocardial anoxia. The first group received 25 mg/kg methylprednisolone sodium succinate i.v. within 4 hr of the onset of chest pain. The second group received propranolol, 5-mg, i.v. within 4 hr of the onset of chest pain. The second group received propranolol, 5-mg, i.v. within 4 hr of the onset of chest pain, and the third group comprised patients who developed AMI while on propranolol therapy and were maintained on this drug after admission to the hospital. All three groups showed an alteration in the pattern of lysosomal and cytosolic enzyme activity and a relative reduction in NAG activity compared to CK-MB.
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PMID:Plasma lysosomal enzyme activity in acute myocardial infarction and the effects of drugs. 699 62