Glycosaminoglycan metabolism following acute myocardial infarction and the effects of intravenous hyaluronidase therapy.
A series of thirteen patients with acute myocardial infarction was studied. In the 12 patients heparinised on admission, there was a fall in serum hyaluronidase activity, free amino sugar and uronic acid levels. This contrasted with a rise in creatine kinase activity. In a single unheparinised patient, the hyaluronidase level rose. This suggests that necrotic cardiac tissue releases hyaluronidase. Any beneficial effects of the local release of hyaluronidase may be minimized by heparin therapy. Study of patients on a trial of intravenous bovine testicular hyaluronidase following acute myocardial infarction could detect no rise in hyaluronidase levels. This confirms previous reports that human serum inhibits bovine testicular hyaluronidase.
D006025:Glycosaminoglycans / Q000378:metabolism*; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D006821:Hyaluronoglucosaminidase / Q000097:blood / Q000627:therapeutic use*; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000378:metabolism
D006025:Glycosaminoglycans; D006493:Heparin; D006821:Hyaluronoglucosaminidase