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)

A number of hemodynamic, pharmacologic and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, external counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (elevation of coronary perfusion pressure by alpha-adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (mannitol, hypertonic glucose); presumably by augmenting anaerobic metabolism (glucose-insulin-potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia) or through reduction of collateral flow (hemorrhagic hypotension, minoxidil) or by decreasing substrate availability glycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin, intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, suggesting that the concept of reduction in infarct size following coronary occlusion is applicable clinically.
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PMID:Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. 0 95

A number of hemodynamic, pharmacologic, and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (evevation of coronary perfusion pressure by alpha adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (manitol, hypertonic glucose); presumably by augmenting anaerobi metabolism (glucose-insulin-potassium, hypertonic glucoxe insulin potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia), through reduction of collateral flow (hemorrhagic hypotension, minoxidil), or by decreasing substrate availability (hypoglycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, which suggests that the concept of reduction in infarct size following coronary occlusion is applicable clinically.
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PMID:Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. 76 15

In anesthetized open chest dogs, hydrocortisone (50 mg/kg body weight administered 30 minutes after occlusion and 25 mg/kg 12 hours later) substantially reduced the size of myocardial infarcts, as reflected by both myocardial creatine phosphokinase activity and histologic appearance 24 hours later. Similarly, hyaluronidase, which increases diffusion through the extracellular space and presumably facilitates delivery of substrate to ischemic cells, also reduced the extent of myocardial necrosis after coronary occlusion in the dog. In view of the salutary effects of hyaluronidase and the absence of serious side effects, this agent was administered clinically to two groups of patients, who were compared with two groups of untreated control subjects. Hyaluronidase (500 National Formulary units/kg X 8) was shown to result in a significantly more rapid reduction in the magnitude and the extent of precordial S-T segment elevations, and in patients treated within 4 hours a tendency to a lower incidence rate of Q waves and a smaller reduction of R waves.
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PMID:Effects of hyaluronidase and hydrocortisone on myocardial necrosis after coronary occlusion. 125 92

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

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

Bovine testicular hyaluronidase (BTH) reduces experimental myocardial infarct size and ameliorates electrocardiographic signs of ischemia. This study was done to determine if heparin, an in vitro inhibitor of hyaluronidase activity, blocks the action of BTH in the myocardium of dogs after coronary artery occlusion. BTH was administered intravenously as 5,000 NF units/kg at 0.5 and 2.5 hours after coronary occlusion. Heparin was administered intravenously as a 150-unit/kg loading dose, followed by 10 units/kg per hour i.v., beginning 15 minutes before coronary occlusion. The area of myocardial ischemia at risk was assessed by a radiolabeled microsphere technique; the area that developed necrosis was assessed by a histochemical technique. In vivo activity of BTH was assessed by a colorimetric analysis of the BTH substrate, i.e., hyaluronic acid (HA), extracted from myocardial tissue. For biochemical analysis of HA, the heart was divided into anterior myocardium, which included ischemic tissue and posterior nonischemic myocardium. The myocardial HA content of dogs treated with BTH plus heparin (anterior, 3.44 +/- 0.40 micrograms HA/mg protein; posterior, 3.69 +/- 0.33 micrograms HA/mg protein) was not significantly different from control (anterior, 3.61 +/- 0.29 micrograms HA/mg protein; posterior, 3.55 +/- 0.23 micrograms HA/mg protein). In contrast, BTH lowered myocardial HA content (anterior, 2.16 +/- 0.21 micrograms HA/mg protein; posterior, 2.08 +/- 0.14 micrograms HA/mg protein) compared with either BTH plus heparin or control groups in both anterior myocardium (p = 0.006) and posterior myocardium (p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin inhibits bovine testicular hyaluronidase activity in myocardium of dogs with coronary artery occlusion. 670 49

The goals of this investigation were: 1) to examine the pattern of evolution of epicardial R wave voltage during the 24 h after experimental coronary artery occlusion; and 2) to determine whether hyaluronidase, an agent shown previously to reduce myocardial ischaemic injury, alters this evolution. Coronary artery occlusion was performed in 36 dogs. In the control dogs, the average R wave voltage (R) recorded over the ischaemic myocardium increased by 7.6 +/- 0.8 mV (P less than 0.001) from before to 15 min after coronary artery occlusion, then gradually returned to baseline over the ensuing 4 h. Subsequently, R wave voltage continued to fall, and 24 h after occlusion, R was 17.8 +/- 1.8 mV (P less than 0.001) less than before occlusion. In the hyaluronidase-treated dogs (500 NF units . kg-1), R recorded over the ischaemic myocardium increased similarly to the controls before hyaluronidase administration. However, in contrast to the control dogs, the administration of hyaluronidase 20 min after occlusion caused R to return to baseline over the ensuing 40 min and 24 h after occlusion, the treated animals lost significantly less R wave voltage than the controls (P less than 0.001).
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PMID:Evolution of epicardial R wave voltage following experimental coronary artery occlusion: effects of hyaluronidase. 730 26