Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.36 (hyaluronidase)
4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ECG, histological, and histochemical examinations on a model of experimental myocardial infarction showed that hyaluronidase administration leads to a decrease in the sum of elevation of the ST segment and the number of points (NST) at which this elevation is recorded, acceleration of healing processes in the affected zone, and to activation of respiratory enzymes and the pentosophosphate shunt in some of the fibres of the peri-infarction zone.
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PMID:[Effect of hyaluronidase on morphological changes in the myocardium in experimental myocardial infarct]. 43 87

Both crude and highly purified testicular hyaluronidase preparations have been shown to contain a component which increases the permeability of the microcirculation in rat skin. This permeability activity had an isoelectric point of 7.4 while hyaluronidase was 9.4. It also could be separated from hyaluronidase by acrylamide gel electrophoresis. The permeability factor was not inhibited by serum and may explain previous observations that hyaluronidase preparations decrease the ischemia and necrosis appropriate to experimental myocardial infarction in vivo.
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PMID:Permeability factor contaminating hyaluronidase preparations. 51 Dec 98

The myocardium of 60 rabbits with experimental myocardial infarction induced by ligation of the anterior interventricular branch of the left coronary artery was studied by electron microscopy. The main group of animals received hyaluronidase. The size of the infarct was judged by the ECG recorded with 15 precordial leads. Normalization of myocytes in the non-ischemic zone of the left ventricle in the treated animals revealed. Better intactness of myocytes in the peri-infarction and non-ischemic zones was noted, which may apparently accelerate ECG dynamics, change the total balance of necrotic material in the direction of its decrease, and, consequently, influence the indices of blood plasma creatine phosphokinase.
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PMID:[Electron-microscopic study of changes in the myocyte ultrastructure under the effect of hyaluronidase in experimental myocardial infarct]. 92 53

The effects on the evolution of canine myocardial infarction (MI) of the lymphagogues hyaluronidase (hyaluronate glucanohydrolase) (known to reduce the size of MIs) and calcium dobesilate (calcium, 2,5-dihydroxybenzenesulfonate, CLS 2210) were compared in a coded, placebo-controlled study in 48 dogs, during the first 24 h after coronary occlusion. MI was induced by embolization of the anterior descending branch of the left coronary artery. The animals were given either a placebo, CLS 2210, or hyaluronidase by intravenous infusion begun immediately after embolization and continued for 24h. The volume of myocardial tissue at risk was evaluated at 2 and 24 h by ungated computed tomography (CT), and after necropsy by staining myocardial sections with triphenyl tetrazolium chloride (TTC). Electrocardiography and estimation of serum creatine kinase (CK) activity were also performed. In the 25 animals that survived 24 h, the results of all tests showed that there was less myocardial damage in the animals treated with the two lymphagogues than in those treated with placebo, and less damage with CLS 2210 than with hyaluronidase. The good correlation between the volume of ischemic tissue as assessed by CT in vivo and as assessed by TTC staining after necropsy (r = 0.959) confirms that the CT perfusion phase defect accurately reflects the volume of tissue at risk during the evolution of MI. This study has shown that CLS 2210 is at least as effective as hyaluronidase in reducing myocardial damage due to coronary artery occlusion in dogs.
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PMID:Myocardial infarction treated with two lymphagogues, calcium dobesilate (CLS 2210) and hyaluronidase: a coded, placebo-controlled animal study. 169 85

Experimental myocardial infarction was induced in rats. The myocardial accumulation of hyaluronan (HA) and water during the development of infarction was measured. The extractable HA content of the infarcted area increased progressively from day 1 and on day 3 reached a threefold increase compared with the HA amounts in myocardium of sham operated controls. The relative water content of infarcted areas also increased progressively reaching a maximum value by day 3 and was strongly correlated with the HA accumulation. Affinity histochemistry visualized a thin rim of HA in the endoperimysium in healthy myocardium. By day 2 an interstitial edema with inflammatory cells was apparent. The widened endoperimysium stained extensively for HA. By its water-binding ability, interstitial accumulation of HA will contribute to the interstitial edema in infarcted myocardial tissue. An interstitial edema is likely to influence the electromechanical characteristics of the myocardium and facilitate reentry phenomena due to a loss of contact between muscle cells. The edema also induces an increased extracellular pressure and an altered myocardial wall compliance that might impair myocardial microcirculation. The findings are relevant to an understanding of the beneficial effect of hyaluronidase treatment in limiting cellular damage during myocardial ischemia.
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PMID:Accumulation of hyaluronan and tissue edema in experimental myocardial infarction. 193 49

Several pharmacological agents possess cardio-protective properties. Some of these agents have been evaluated in the context of the limitation of the size of the myocardial infarction. In this study, controlled randomised trials evaluated the effects of a solution of glucose-insulin-potassium (GIK), hyaluronidase, nitrate derivatives, calcium antagonists and beta-blockers administered during the first few hours following acute myocardial infarction. Despite promising results, we do not yet have any proof of the effectiveness of the GIK solution, hyaluronidase or nitrate derivatives. Nifedipine appears to be devoid of any effect and other calcium antagonists are currently under investigation. The numerous trials have been performed with beta-blockers generally support their beneficial effect on the limitation of the size of the infarction, which is usually accompanied by a reduction in the mid and long term mortality. They are therefore recommended in this indication and their practical use is discussed.
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PMID:[Pharmacologic limitation of the size of the myocardial infarction (excluding thrombolysis)]. 286 26

Theoretically, interventions that restore the balance between oxygen supply and demand when given during the early hours of a heart attack may reduce infarct size and prevent fatal arrhythmias and thereby prolong survival. Data on mortality from the available randomized trials of thrombolytic therapy, intravenous beta blockers, hyaluronidase, intravenous nitrates and calcium channel blockers in acute myocardial infarction, are systematically reviewed. Analyses confirm that intravenous streptokinase reduces mortality by about 25% but suggests that measures to prevent reinfarction may be required after thrombolytic therapy. beta blockers reduced mortality by approximately 15%. The pooled data from the existing trials of hyaluronidase and intravenous nitrates are consistent with a 15% to 20% decrease in mortality; ideally this should be confirmed in future large randomized trials. Currently, there is no evidence either from individual studies or the aggregate of all the trials that calcium channel blockers reduce mortality. The collective experience from the trials carried out over the last 2 decades suggests that most interventions in acute myocardial infarction have, at best, only moderate effects with a 10% to 20% reduction in mortality. Current and future trials that assess the effects of cardiovascular treatments on mortality should therefore aim to randomize 10,000 to 20,000 average risk patients or a few thousand high risk patients.
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PMID:Interventions that potentially limit myocardial infarct size: overview of clinical trials. 288 96

GL enzyme (hyaglosidase) is a highly purified component enzyme of hyaluronidase. A therapeutic trial was carried out in the treatment of suspected myocardial infarction among 1,488 patients presenting within 6 h of the onset of symptoms. No significant reduction in mortality at 6 months was observed in the GL group (15.7%) compared with the placebo group (16.4%). Mortality at 2 weeks was also unaffected by treatment (GL 10.3%; placebo 10.9%).
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PMID:A controlled trial of GL enzyme in the treatment of acute myocardial infarction. 304 47

During the course of experimentally induced myocardial ischaemia affected tissue initially suffers reversible ischaemic injury or, if ischaemia persists, injury of increasing severity before becoming irreversibly damaged. This state is characterized by tissue necrosis and referred to as myocardial infarction. The purpose of this study was to investigate whether it is possible to delay or perhaps even prevent the development of irreversible ischaemic injury. Ischaemia was induced by coronary artery occlusion (CAO) in canine hearts for 90 min or 24 h. The drug used for intervention was hyaluronidase. Ischaemic damage was assessed by p-NBT staining and ultrastructural evaluation of tissue biopsies. Development of irreversible ischaemic damage was prevented during 90 min of CAO. However, progression of reversible to irreversible ischaemic injury could not be prevented during 24 h of CAO. In conclusion, it is possible to prevent the development of irreversible ischaemic injury by a suitable intervention during the early stages of ischaemia in the canine heart and thus to gain time for additional intervention in the early treatment of myocardial infarction.
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PMID:Delay of development of transmural irreversible ischaemic injury in canine myocardium. 311 45

To assess whether a cardiac lymphagogue, CLS 2210, would reduce myocardial infarct size after coronary artery ligation, studies were performed in 14 dogs. The left anterior descending coronary artery was ligated in each dog, and the dogs were randomized to either placebo or CLS 2210 treatment, which was carried on for seven days. After seven days the animals were sacrificed and the volume of infarcted myocardium was determined macroscopically on a double-blind basis, supported by histologic examination. CLS 2210 treatment resulted in a highly significant reduction in the volume of infarcted myocardium (p less than 0.001). Since CLS 2210 is chemically and pharmacologically unrelated to hyaluronidase but shares an action with hyaluronidase as a cardiac lymphagogue, the results offer further support for a role of myocardial lymphatics in the evolution of myocardial necrosis following coronary artery occlusion and provide an explanation for the mechanism by which these agents reduce myocardial infarction size.
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PMID:Salvage of ischemic myocardium by CLS 2210 in the dog: a preliminary double-blind study. 354 69


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