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)

The effect of hyaluronidase on the early course of acute myocardial infarction was evaluated in closed chest anesthetized pigs. One hour after balloon catheter occlusion of the left anterior descending coronary artery, hyaluronidase (500 units/kg body weight) was rapidly infused in 10 animals while 9 received no treatment. The animals were than observed over the next 4 hours. Cardiac output, heart rate, mean arterial pressure and left atrial pressure were not significantly affected by treatment. Heart rate increased and arterial pressure decreased in each group to a comparable degree of 5 hours, but left atrial pressure and cardiac output were unaffected. Precordial S-T segment mapping revealed no significant difference between the two groups. S-T segments rose to a comparable degree in each group and peaked before 1 hour. Hyaluronidase had no acute effects on the S-T segment map in the first 30 minutes after infusion or during the subsequent return of the map toward control level. Slightly lower S-T segments in the hyaluronidase-treated group at 5 hours was of borderline significance but was attributed to factors other than the drug intervention. Changes in ventricular wall motion were assessed angiographically, and all animals manifested akinetic or dyskinetic segments. A significant reduction in shortening fraction of involved segments was seen after occlusion, but no difference was observed between the two groups at 5 hours. Shortening fraction of the combined anterior and anteropical segments decreased from 66 +/- 10 to 20 +/- 6 percent at 5 hours in the hyaluronidase group (no. = 7) whereas in the control group (no. = 6) it decreased from 68 +/- 6 to 28 +/- 9 percent. Comparable increases in end-diastolic volume were also present at 5 hours in each group. Volumes increased from 80.6 +/- 5.1 to 97.5 +/- 6.4 ml3 at 5 hours (P less than 0.05) in the hyaluronidase-treated group (no. = 10) compared with 86.9 +/- 8.9 to 104.8 +/- 11.0 ml3 (P less than 0.05) in the control group (no. = 8). Hyaluronidase did not alter the early course of acute myocardial infarction in pigs. Species differences may contribute to different results reported to date.
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PMID:Failure of hyaluronidase to alter the early course of acute myocardial infarction in pigs. 94 84

The effect of hyaluronidase on myocardial ischemic injury was examined in 13 patients with acute myocardial infarction, and the results were compared with 11 patients who did not receive hyaluronidase. A 35-electrode precordial mapping method was used to assess the rate of resolution of ST segment elevations. In the 11 control patients, the sum of ST segment elevations (sigmaST) fell after 2 hours to an average of 93.5% plus or minus 17.3% (SEM) and after 24 hours to 89.6% plus or minus 7.6% of the initial values, while the number of electrodes exhibiting ST segment elevations exceeding 0.1 mV (NST) fell to 98.0% plus or minus 12.3% and 94.3% plus or minus 10.4% of the initial values respectively. In the hyaluronidase-treated group, at the same time sigmaST fell significantly more (P less than 0.05), to 54.1% plus or minus 5.0% and 51.3% plus or minus 11.8% and NST was also more markedly reduced (P less than 0.05) to 50.7% plus or minus 7.8% and 50.1% plus or minus 12.4%, thus indicating that hyaluronidase can accelerate the reduction of myocardial ischemic injury in patients with acute myocardial infarction.
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PMID:Effects of hyaluronidase administration on myocardial ischemic injury in acute infarction. A preliminary study in 24 patients. 111 65

In this article, data on mortality have been systematically reviewed from the randomized trials of intracoronary and intravenous (i.v.) thrombolytic therapy, hyaluronidase, i.v. nitrates, and calcium channel blockers in acute myocardial infarction (AMI). Such analyses confirm that i.v. streptokinase (SK) reduces short-term mortality by about 20%. Despite a higher incidence of reinfarction in the treated group, this early benefit is maintained long term. The excess reinfarction was observed whether or not SK was followed by anticoagulants or aspirin. The roles of pharmacologic interventions and percutaneous transluminal coronary angioplasty (PTCA) in preventing reinfarction and improving survival further are currently being evaluated. The pooled data from the existing trials of hyaluronidase and i.v. nitrates are consistent with a 20-30% reduction in mortality; ideally, these interventions should also be studied 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 these trials conducted over the last two decades suggests that most interventions in AMI can at best have only moderate effects (10%, 20%, or at best 30%) on mortality. However, such modest effects produced by the widespread use of these agents could prevent several thousand premature deaths each years. Therefore, current and future trials that assess the effects of new or existing cardiovascular treatments on mortality should aim to randomize at least 10,000 average risk patients or a few thousand high risk patients.
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PMID:An overview of the clinical trials of agents (other than beta-blockers) that potentially limit myocardial infarct size. 246 35

The present study compares the protective effects of sodium selenite (Se), hyaluronidase (Hy) and anisodamine (An) on infarct size, left ventricular myocardial contractility (LVMC) and relaxation (LVMR) and myocardial hypertrophy on the 3rd, 9th and 21st days after the ligation of left main coronary artery in the rats. The results showed that Se could reduce the infarct size, so could Hy and An. However, Se could relevantly improve LVMC and LVMR at the acute phase of infarction, while Hy and An could not. On the 21st day (healing phase) of infarction the indexes of the LVMC and LVMR in Se-, Hy- or An-treated rats were significantly better than those in the control rats. Se could enhance the extent of hypertrophy in non-infarcted myocardium, while Hy and An could not. On the 21st day of this experiment the total natural mortality in the Se-treated rats was significantly lower than that in the control or in the An-treated rats. These data suggest that Se is superior to Hy and An in the treatment of acute myocardial infarction.
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PMID:Protective effects of sodium selenite on experimental myocardial infarction. 256 Sep 57

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

A randomized, double-blind, multicenter study was conducted of the value of hyaluronidase therapy for acute myocardial infarction (AMI). Patients were eligible for enrollment if they were less than 76 years old, had at least 30 minutes of pain typical of myocardial ischemia and had electrocardiographic changes suggestive of acute ischemia or evolving infarction. A total of 851 patients were randomly assigned to hyaluronidase (500 National Formulary units/kg intravenously every 6 hours for 48 hours) or placebo therapy with a mean of 9.4 +/- 0.1 hours after the onset of pain. There were no significant differences between the hyaluronidase- and placebo-treated patients in incidence of AMI (86 vs 88%), creatine kinase-MB infarct size index (14.6 +/- 0.8 vs 15.1 +/- 0.7 CK-MB-gEq/m2), change in total R wave from time 0 to 72 hours for anterior transmural ischemia or infarction (-34 +/- 7 vs -35 +/- 8 mV), infarct size determined by pyrophosphate scintigrams (27 +/- 1 vs 27 +/- 1 cm2), change in left ventricular ejection fraction from day 0 to day 10 (+ 2.4 +/- 0.7 vs + 1.2 +/- 0.7%) or cumulative proportion surviving 4 years (0.70 +/- 0.03 vs 0.68 +/- 0.03). These findings indicate there is no overall benefit from administration of hyaluronidase more than 9 hours after the onset of AMI, but do not exclude the possibility that such therapy could be of value if given earlier, or if given to a subgroup of patients with sufficient residual flow to the area of AMI.
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PMID:Hyaluronidase therapy for acute myocardial infarction: results of a randomized, blinded, multicenter trial. MILIS Study Group. 287 94

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

A multicentred, randomised, blind study was started in 1978 to compare propranolol or hyaluronidase with placebo in patients with acute myocardial infarction admitted within 18 hours of onset of symptoms. Patients were randomised to group A and received hyaluronidase, propranolol, or placebo, or, if propranolol was contraindicated, to group B and received hyaluronidase or placebo. Hyaluronidase (500 U/kg given every six hours for 48 hours) had no effect on mortality or infarct size in the overall population. Because spontaneous reperfusion was more common in patients with early peaking of plasma creatine kinase MB or non-transmural electrocardiographic changes or both, the results were reanalysed for two subgroups: those in whom plasma creatine kinase peaked less than 15 hours after the onset of symptoms (early peak, n = 184) and those with a peak greater than 15 h after the onset of symptoms (late peak, n = 546). The distribution of time to peak activity of creatine kinase MB was similar in the hyaluronidase and placebo groups. In the early peak patients who were given hyaluronidase (groups A and B) total mortality and cardiac-specific four year mortality were significantly lower. This was most pronounced in group B in which the total mortality was 45% and cardiovascular mortality was 47% less than in the placebo group. Similarly, mortality from cardiovascular disease in patients (groups A and B) with nontransmural ischaemia (ST-T changes) given hyaluronidase was significantly lower, with group B showing a 50% reduction. In the subsets of patients with late peaking of creatine kinase MB or those presenting with transmural electrocardiographic changes there was no difference in total mortality or deaths from cardiac disease between those given hyaluronidase and those given placebo. Hyaluronidase was associated with improved survival in patients with early peaking of plasma creatine kinase MB, suggesting the possibility of salvage of myocardium in patients who have early spontaneous reperfusion and possibly after therapeutic reperfusion.
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PMID:Effect of hyaluronidase on mortality and morbidity in patients with early peaking of plasma creatine kinase MB and non-transmural ischaemia. Multicentre investigation for the limitation of infarct size (MILIS). 305 76

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

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


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