Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the past decade, efforts to limit the extent of myocardium exhibiting infarction once ischemia has been initiated have focused on manipulation of myocardial oxygen supply and demand as well as the process of injury itself. Interventions of promise range from the conventional, moderate increase in inspired oxygen content, to administration of hyaluronidase or intracoronary thrombolysis to augment oxygen supply; use of beta-adrenergic blocking drugs and nitroglycerin to diminish demand; and administration of calcium antagonists and prostaglandin synthesis inhibitors to limit the injury process. The ultimate effects on infarct size and long-term mortality have yet to be established unequivocally for any of these approaches in the clinical setting of acute myocardial infarction, but significant preservation of ischemic myocardium with hypothermia and with administration of nifedipine during coronary-artery bypass surgery have been documented. Several prospective, large-scale, blinded, and random sample selection clinical trials are currently in progress. Their results should definitively elucidate the clinical utility of specific interventions under defined conditions and should help to further improve the management of patients with ischemic heart disease.
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PMID:Pharmacological salvage of myocardium. 612 93

Several substances have been claimed to be effective in reducing the area of necrosis in acute myocardial infarction. The effects of a highly purified hyaluronidase preparation (Hyalas) on experimental myocardial infarction in the rat have been evaluated in this study. In the first series, one group of rats was treated with hyaluronidase 1 500-2 000 IU/kg injected intravenously 2, 4, 18, 24, 28 and 42 hours after induction of infarction by coronary artery occlusion. Another group was treated with NaCl solution. The infarction size was evaluated by serum lactate dehydrogenase and weight of infarcted myocardium. In a second series, the substances were administered immediately after the occlusion. In this experiment, the infarction size was estimated by planimetry. The percentage of salvaged myocardium in the hyaluronidase-treated groups was within the range of 20%. It seems reasonable to suggest that the use of highly purified hyaluronidase may be of clinical value for reduction of the myocardial infarction size.
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PMID:The effects of a highly purified hyaluronidase preparation on experimental myocardial infarction in the rat. 649 78

There is experimental and clinical evidence that i.v. injection of bovine testicular hyaluronidase (BTH) reduces the extent of necrosis during myocardial infarction. The fate of i.v. administered BTH has not been described. In this study, serum kinetics of BTH enzyme activity in dogs, rats and humans were determined. Tissue distribution of BTH was determined with an 125I-labeled preparation of purified BTH. Serum BTH activity initially decreased exponentially with half-life 2.0 +/- 0.1 min in dogs with coronary artery occlusion (n = 8; 500 U of BTH/kg); 3.2 min in humans with acute myocardial infarction (n = 2; 500 U of BTH/kg); and 3.2 +/- 0.3 min in rats (n = 5; 5,000 U of BTH/kg). In dogs BTH disappearance showed two distinct phases. After injection of high dose BTH (5,000 U of BTH/kg), during the first 7 min serum half-life of BTH was 2.1 +/- 0.2 min (n = 8), but increased to 9.4 min in later serum samples. After the injection of 125I-labeled BTH into the rat, protein-bound 125I disappeared from serum with a half-life (3.4 min) that is similar to the serum half-life of BTH enzyme activity (3.2 min). Twenty minutes after injection of 125I-labeled BTH, 30% of the label was recovered in the liver. It is concluded that BTH activity has a short serum half-life of less than 10 min in dogs, rats and humans. In the rat model, the disappearance of serum BTH activity results from physical removal of circulating BTH molecules rather than serum inhibition or inactivation of BTH enzymatic activity.
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PMID:The serum kinetics of bovine testicular hyaluronidase in dogs, rats and humans. 709 53

Using a very sensitive new technique, the effectiveness of hyaluronidase (HYL) in reducing infarct size (IS) was compared employing HYL obtained from bovine testicles and from fungi. One minute after coronary artery occlusion in dogs, highly radioactive microspheres were injected for autoradiographic assessment. The animals were then randomized into a control group and several HYL-treated groups. Six hours later all hearts were divided into 20 to 25, 3 mm-thick slices which were incubated in TTC to measure IS and thereafter autoradiographed to delineate the hypoperfused zone (HZ). The percent of HZ that evolved to necrosis (IS/HZ) was determined in each animal. In the control group, IS/HZ was 89.9 +/- 4.2% and was reduced by 17% (p less than 0.05) in the group treated with 500 units/kg of bovine HYL. With 500 units/kg of fungal HYL, IS/HZ was not reduced, but the higher dose of 5000 units/kg reduced IS/HZ by 26% (p less than 0.01). Thus dependence of HYL source is documented relative to the effectiveness of this salutary intervention for protecting ischemic heart muscle and limiting necrosis in acute myocardial infarction.
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PMID:Importance of the source of hyaluronidase preparations in determining protective effect on ischemic heart muscle in acute myocardial infarction. 719 83

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.
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PMID:Glycosaminoglycan metabolism following acute myocardial infarction and the effects of intravenous hyaluronidase therapy. 738 76


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