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)

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

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

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

Earlier studies have shown that hyaluronidase exerts a potent influence upon the lymphatic system of the myocardium and that it reduces the size of myocardial infarcts after coronary occlusion. In this study we compared, in mongrel dogs, the effect of intravenous hyaluronidase or CLS 2210 upon the cardiac lymphatic vessels. We observed that in CLS 2210-treated animals the number of visualized cardiac lymphatic vessels was significantly higher than in the hyaluronidase-treated control group. We have previously demonstrated a cardioprotective effect of hyaluronidase in the treatment of acute myocardial infarction. The present experimental data indicate that intravenous CLS 2210 may have a definite role in the management of acute coronary occlusion. Further studies are needed to confirm these preliminary findings.
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PMID:CLS 2210, hyaluronidase and the cardiac lymphatic system. 383 39