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)

Cartilaginous and/or osseous foci were observed in eight aortas from 20 rabbits immunized against heterologous aorta homogenates and sacrificed 11 to 24 months later. They were studied by means of histological and histochemical methods and compared with normal aortas, cartilage and bone. Some of the observed changes seemed to be true markers of these transformations. Chondroid metaplasia was characterized by 1) generalized increase in alcianophilic hyaluronidase sensitive substances. 2) Appearance of Dermatan and/or Keratan sulfates round some isolated cells. 3) Advent of G6 Pase and Alk. Phase activities in cells adjacent to osseous foci. Osteous metaplasia was characterized by 1) decrease, then disappearance of alcianophilic and PAS positive material, 2) increase in osteoblastic alkaline Pase-activities.
Basic Res Cardiol
PMID:Cartilage and bone formation in arterial wall. 1. Morphological and histochemical aspects. 12 Dec 37

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.
Am J Cardiol 1976 Jul
PMID:Failure of hyaluronidase to alter the early course of acute myocardial infarction in pigs. 94 84

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.
Am J Cardiol 1976 Mar 31
PMID:Effects of hyaluronidase and hydrocortisone on myocardial necrosis after coronary occlusion. 125 92

Experiments were performed to determine the cellular associations of the molecular forms of acetylcholinesterase (AChE) in adult rat heart. For this purpose, a cardiac muscle and a non-muscle fraction were isolated from rat heart ventricles after perfusion with collagenase and hyaluronidase, extracts of these fractions were subjected to ultracentrifugation on linear density gradients of sucrose (5-20%), and fractions of these gradients were analyzed for AChE activity. The results show that only globular AChE molecular forms were present in isolated cardiac muscle cells. Globular AChE forms were also present in the non-muscle cells fraction but in different proportions. The proportions of globular AChE forms plus the high specific activity of choline acetyltransferase in the non-muscle cell fraction suggest that this fraction contains cholinergic nerve fragments. The results of this study also show that asymmetric AChE is released during the perfusion of heart with the digestive enzymes, which suggests that asymmetric AChE is bound to the extracellular matrix of heart.
J Mol Cell Cardiol 1989 Oct
PMID:Acetylcholinesterase molecular forms in muscle and non-muscle cells of rat heart. 258 21

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.
Ann Cardiol Angeiol (Paris)
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.
Am J Cardiol 1986 Jun 01
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.
Am J Cardiol 1987 Jul 15
PMID:Interventions that potentially limit myocardial infarct size: overview of clinical trials. 288 96

Myocytes were isolated by Langendorff perfusion of rat or rabbit hearts with low calcium solution followed by collagenase and hyaluronidase, or by incubation of chunks of rat ventricular tissue in similar media. Cells were then placed in a bath on a microscope stage, superfused and electrically stimulated. Contraction amplitude and rate of change of length during contraction were measured using a video camera and edge detection monitor. Cells were selected for study using a number of criteria developed to identify and define a cell population able to give consistent inotropic responses over a long period. The maximum contraction amplitude with isoproterenol in rabbit cells was 0.244 micron (sarcomere length change) or 13.1% (percentage change in cell length), and the EC50 was 12.8 nM. The maximum contraction amplitude with isoproterenol did not differ significantly between rat and rabbit, between cells prepared by perfusion and those made from chunks, or when determined from non-cumulative rather than cumulative curves. The EC50 for isoproterenol in rat cells made by the perfusion method (cumulative curves) was 3.81 nM, significantly lower than in rabbit. The maximum amplitude obtained with increasing concentrations of calcium was not significantly different from that with isoproterenol under any condition. The EC50 for calcium averaged 2.78 mM in rat cells made by the perfusion method (cumulative curves) and was significantly greater than that in rabbit (1.4 mM). Maximum rates of contraction for rat cells averaged 4.59 micron/s in 8 mM calcium. Rat cells contracted faster than they relaxed, whereas rabbit cells in 8 mM calcium relaxed faster than they contracted. Rat cells, maximally activated by either calcium or isoproterenol, contracted significantly faster than rabbit. There was no difference in rates of contraction (or relaxation) between rat cells prepared by perfusion and those made from chunks of tissue.
J Mol Cell Cardiol 1988 Jul
PMID:Contractile responses of isolated adult rat and rabbit cardiac myocytes to isoproterenol and calcium. 317 50

Adult rat heart was dissociated into a single-cell suspension by a retrograde perfusion technique with collagenase and hyaluronidase in Krebs-Ringer phosphate buffer. Long-term culture of these isolated single cardiac muscle cells was established for up to 45 days. Transmission electron microscopy and immunofluorescence analysis with monoclonal antibodies to cardiac myosin were used to examine sequentially the external and internal structural organization of the cardiac myocytes. Most of the cardiac myocytes exhibited prominent alterations in their external and internal structural organization during the first two weeks of culture. As they attached to the substrate and spread out, the myocytes assumed various shapes and sizes, with the exception of a few which maintained their original cylindrical shape. Electron microscopy of 2 to 4-day cultures revealed that most of the muscle cells contained disorganized myofibrils and surface blebs with enclosed mitochondria and myofilaments, which were eventually extruded from the cytoplasm. With progressive culture, the cardiac myocytes appeared to lose myofibrillar material; fewer myofilaments or sacromere fragments with interfibrillar mitochondria were observed in the sarcoplasm. Such cells resembled cultured embryonic or neonatal cardiac myocytes. However, some muscle cells retained closely packed, well organized myofibrils characteristic of freshly dissociated or in vivo cardiac myocytes. Immunofluorescence microscopy demonstrated that the cultured cardiac myocytes were strongly myosin positive throughout their morphological changes and subsequent maintenance in culture. Two patterns of fluorescence were observed in these cells in correlation with the fine structural evidence for myofibrillar distribution. One pattern exhibited bright fluorescence near the central region of the cell with a more weakly diffuse fluorescence throughout the cytoplasm; the other pattern was characterized by bright fluorescence throughout the sarcoplasm. Most of the myocytes retained their contractility throughout the culture period excepting the initial 24 to 48 h of cell attachment and flattening. These studies demonstrate the feasibility of maintaining contractile cardiac muscle cells from adult rats for at least 1 1/2 months in monolayer culture, although some variability in myofibrillar organization has been observed.
J Mol Cell Cardiol 1983 May
PMID:Long-term cell culture of adult mammalian cardiac myocytes: electron microscopic and immunofluorescent analyses of myofibrillar structure. 635 Jun 10

Over a 34.5-month period, all admissions to 5 university hospital coronary care units were screened for eligibility for the Multicenter Investigation of the Limitation of Infarct Size (MILIS), an ongoing study of the effects of hyaluronidase, propranolol and placebo on myocardial infarct (MI) size. Of 3,697 patients with greater than or equal to 30 minutes of discomfort that was thought to reflect myocardial ischemia who were assessed for the presence or absence of certain electrocardiographic abnormalities at the time of hospital admission, the electrocardiogram was considered predictive of acute MI if greater than or equal to 1 of the following abnormalities was present: new or presumably new Q waves (greater than or equal to 30 ms wide and 0.20 mV deep) in at least 2 of the 3 diaphragmatic leads (II, III, aVF), or in at least 2 of the 6 precordial leads (V1 to V6), or in I and aVL; new or presumably new ST-segment elevation or depression of greater than or equal to 0.10 mV in 1 of the same lead combinations; or complete left bundle branch block. In the screened population, the diagnostic sensitivity of the electrocardiographic criteria was 81%, whereas the overall infarct rate in the total population screened was 49%. The diagnostic specificity of these entry criteria was 69% and the predictive value 72%.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1983 Nov 01
PMID:Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3,697 patients. 635 62


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