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)

The effects of the intravenous administration of hyaluronidase (HY; 2,500 IU/kg) and urokinase (UK; 20,000 and 40,000 IU/kg), alone or in combination, on the isoproterenol (ISP) induced myocardial infarction (MI) in rats, were studied. The severity of infarction was determined by measuring the levels of serum enzymes (CPK, GOT, LDH) and by evaluating the extent of the injured areas and the incidence of mortality. Plasma thromboxane B2 (TXB2) levels were also determined. All the treatments reduced the infarction area and the enzyme levels (increased by ISP) to a varying degree. However, a definite potentiating activity was obtained when HY was combined with the highest dose of UK. This combination was also capable of reducing the mortality rate. Finally, both HY and UK or the combined preparation brought the plasma TXB2 levels back to normal. These findings suggest the possibility of complementary activities of HY and UK in the treatment of experimental MI.
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PMID:The co-operative action of hyaluronidase and urokinase on the isoproterenol-induced myocardial infarction in rats. 371 99

To assess myocardial lymphatics during the evolution of myocardial infarction we performed lymphangiographic studies thirty and three hundred sixty minutes after occlusion of the left anterior descending coronary artery in 92 dogs. A morphometric index was employed on a coded basis to assess the lymphangiograms. Well before myocardial necrosis was evident, at thirty minutes, a striking reduction was evident in lymphatic filling in the ischemic zone: similar changes were seen three hundred sixty minutes after occlusion. Heparin in doses that rendered blood incoagulable did not prevent the lymphatic occlusion or collapse, but they were prevented by two agents that act as cardiac lymphagogues, hyaluronidase and CLS 2210. Lymph flow from the heart was assessed in another 23 dogs. Lymph flow fell sharply after coronary artery occlusion in placebo-treated dogs but was well maintained in dogs treated with hyaluronidase and with CLS 2210. The reduction in cardiac lymphatic filling and lymph flow occurred too early to be a consequence of myocardial necrosis. To the extent that reduced lymphatic drainage allows the local accumulation of potentially toxic products, it could contribute to the local damage. Treatment with the lymphagogues not only maintained lymphatic patency but also reduced evidence of myocardial damage evident on examination by light and electron microscopy. These studies provide an alternative to commonly held concepts on how hyaluronidase reduces myocardial infarction after coronary artery occlusion and support the concept that lymphatic occlusion or collapse plays a role in myocardial infarction.
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PMID:Early disappearance of lymphatics draining ischemic myocardium in the dog. 381 24

The induction of myocardial infarction in rats by ligation of the left-anterior coronary artery was confirmed by measurement of increased plasma levels of creatine kinase, aspartate aminotransferase and lactate dehydrogenase. Using this model system it has been established that intravenous administration of 125I-labelled hyaluronidase to rats resulted in a preferential uptake of the enzyme by damaged myocardium as compared to normal heart tissue.
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PMID:Preferential uptake of intravenously administered hyaluronidase (Hyalosidase) by damaged rat myocardium. 402 52

Throughout the last decade, multiple interventions have been shown to decrease myocardial ischemic injury and limit infarct size in animal models of acute myocardial infarction. Results of pilot studies have suggested that some of these interventions may also have beneficial effects in humans with evolving myocardial infarction. This review focuses on the rationale for limiting infarct size, efficacy of methods for estimating size of infarcts, and current clinical data on specific intervention therapy. No intervention has yet been proved sufficiently efficacious to warrant its routine clinical use. However, treatment with beta-adrenergic blockers, intravenous nitroglycerin, and hyaluronidase has been shown to affect one or more indexes of infarct size in patients with acute myocardial infarction. Large, randomized clinical trials of these and other promising interventions are underway and will provide data on whether infarct size can be limited in humans and whether residual cardiac function and patient prognosis can thereby be improved.
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PMID:Efforts to limit the size of myocardial infarcts. 611 84

79 patients with suspected myocardial infarction entered a randomised trial to establish the safety of early intravenous administration of a highly purified hyaluronidase preparation (GL enzyme) and to assess its effects on eventual infarct size as measured by electrocardiographic, enzymatic, and scintigraphic criteria. Of the 71 patients with infarction, 35 received GL enzyme and 36 placebo within 6 h of the onset of chest pain. GL enzyme injected into a peripheral vein produced no adverse changes in the clinical, haemodynamic, biochemical, or haematological variables studied. GL enzyme reduced precordial electrocardiographic indices of infarct size as reflected by a diminution (p less than 0.02) in the degree of both R wave loss and Q wave development. In addition, the number of leads developing pathological Q waves (N delta Q greater than or equal to 2), a sign of progression from ischaemia to necrosis, was reduced (p less than 0.05) after GL enzyme treatment. However, there were no significant differences in infarct size as measured by cumulative creatine kinase MB isoenzyme release or technetium-99m pyrophosphate scintigraphic infarct area, or in clinical outcome during the hospital stay. Interpretation of the enzymatic and scintigraphic data was complicated by chance bias in pre-treatment randomisation which resulted in more (p less than 0.05) patients with severe haemodynamic impairment (and hence probably larger infarct sizes) entering the GL enzyme group. Nonetheless, a favourable effect of GL enzyme on infarct size was demonstrated by precordial electrocardiographic QRS mapping, here each patient acts as his or her own control.
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PMID:Effects of early administration of a highly purified hyaluronidase preparation (GL enzyme) on myocardial infarct size. 612 98

The influence of intravenous GL enzyme (hyaluronidase) on the outcome of myocardial infarction was assessed in a controlled trial among 483 patients presenting within 6 h of the onset of symptoms. There was a consistent trend towards reduced mortality throughout the period of follow-up among GL enzyme treated patients. When the fate of all patients entering the trial was considered, irrespective of final diagnosis, the reduction in mortality at 6 months (27 of 240 GL enzyme patients, 45 of 243 placebo) was statistically significant (p = 0.025).
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PMID:Effect of GL enzyme (a highly purified form of hyaluronidase) on mortality after myocardial infarction. 612 99

A highly purified preparation of hyaluronidase (GL enzyme) was given in a double-blind, placebo-controlled, randomised study to 192 consecutive patients within 12 h of suspected myocardial infarction. Compared with those receiving placebo, patients with definite myocardial infarction given GL enzyme had significantly less change in QRS complexes; in those with anterior infarction the development of Q waves was less prominent. At 4 months the overall mortality among those with definite and possible myocardial infarction receiving GL enzyme (6 out of 83 patients, 7.2%) was lower than that in those receiving placebo (11 out of 79, 14%); this difference was not significant. No adverse effects were observed.
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PMID:Effect of a highly purified hyaluronidase preparation (GL enzyme) on electrocardiographic changes in acute myocardial infarction. 612

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

Hyaluronidase has been shown clinically and experimentally to reduce the effects of tissue ischemia in myocardial infarction and hemorrhagic shock. Dimethyl sulfoxide (DMSO) has been shown to reverse the effects of cerebral ischemia in the primate model. A caudally based dorsal skin flap in the rat was used to study the effects of these two drugs in physiological doses on skin flaps, and to investigate their mechanisms of action. This study demonstrates that both hyaluronidase and DMSO, which are nontoxic in physiological doses, can increase the surviving length of an experimental skin flap. It is hypothesized that these substances exert their effect by decreasing tissue edema and by aiding in the transport of nutritive substances to the flap during its acute phase.
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PMID:The effect of hyaluronidase and dimethyl sulfoxide (DMSO) on experimental skin flap survival. 663 21

Patients with their first myocardial infarction not initially complicated by severe atrioventricular block or power failure were given a skin test and then randomized to receive either hyaluronidase or placebo in double-blind fashion. Hyaluronidase, 500 IU/kg i.v., was given every 6 hours for 42 hours. Of the 48 eligible patients, 26 received hyaluronidase and 22 received placebo. The mean CK serum entry was 3140 +/- 2111 mIU/ml (mean +/- SD) in hyaluronidase patients and 3574 +/- 1476 mIU/ml in placebo patients (p less than 0.21). The mean infarct size was 54.6 +/- 35.8 CK gram-equivalents in the hyaluronidase patients and 64.0 +/- 31.1 CK gram-equivalents in the placebo patients (p less than 0.20). Among the 21 patients treated within 6 hours of the onset of infarction, the difference in infarct size was greater (p less than 0.15). There was no significant difference in the incidence of power failure, ventricular arrhythmias, recurrence of ischemic pain, infarct extension or mortality. No benefit of hyaluronidase was demonstrated in this study, which was designed to detect a 50% reduction of infarct size. However, to detect a 20% reduction in infarct size would require a much larger study population.
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PMID:Intravenous hyaluronidase therapy for myocardial infarction in man: double-blind trial to assess infarct size limitation. 706 Feb 55


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