acid-phosphatase and Myocardial-Infarction

Topics: Acid Phosphatase; Alkaline Phosphatase; alpha-Amylases; Biliary Tract Diseases; Clinical Enzyme Tests; Enzymes; Female; gamma-Glutamyltransferase; Humans; Isoenzymes; L-Lactate Dehydrogenase; Lipase; Liver Diseases; Metabolism, Inborn Errors; Myocardial Infarction; Nucleotidases; Pancreas; Transaminases; Uterine Neoplasms

Topics: Acid Phosphatase; Adrenal Cortex Hormones; Animals; Cardiomegaly; Cathepsins; Centrifugation, Density Gradient; Coronary Disease; Fasting; Heart Diseases; Heart Failure; Hormones; Humans; Hyperthyroidism; In Vitro Techniques; Liver; Lysosomes; Myocardial Infarction; Myocardium; Thyroxine

Topics: Acid Phosphatase; Aged; Carcinoma; Cardiovascular Diseases; Cerebrovascular Disorders; Clinical Trials as Topic; Diethylstilbestrol; Electrocardiography; Heart Failure; Humans; Ischemia; Male; Myocardial Infarction; Neoplasm Metastasis; Placebos; Plasminogen; Prognosis; Prostate; Prostatic Neoplasms; Pulmonary Embolism

This study was undertaken to determine the association between serum tartrate-resistant acid phosphatase 5a (TRACP5a) and cardiovascular disease (CVD) risk.. Four hundred patients were enrolled including, 291 asymptomatic subjects grouped by the number of traditional risk factors, 36 patients undergoing cardiac arteriography, 34 undergoing percutaneous cardiac intervention, and 39 with acute myocardial infarction. Serum was collected at baseline and, in arteriograpy and intervention groups, periodically for 1 week afterward. In addition to laboratory and clinical evaluation for risk assessment, serum TRACP5a, C-reactive protein (CRP) and interleukin-6 (IL-6) were determined.. All biomarkers rose with increasing CVD risk. Only serum TRACP5a, logCRP and cholesterol were elevated in symptomatic patients. Serum TRACP5a was higher in men and correlated with age, logCRP, logIL-6 and log-triglycerides, and in symptomatic patients, with the number of diseased coronary arteries. IL-6 and CRP showed acute phase responses, whereas TRACP5a did not change over 1 week after arteriography or intervention. After adjustment for all other variables and risk factors, TRACP5a and logCRP were the only biomarkers to associate with symptomatic disease. TRACP5a was more specific than CRP to predict myocardial infarction among all subjects.. Serum TRACP5a is a macrophage-derived inflammation marker associated with CVD risk, and with coronary vessel disease and its severity and may be a useful marker for screening and assessment of CVD risk.

Topics: Acid Phosphatase; Adult; Aged; Aged, 80 and over; Asymptomatic Diseases; Biomarkers; Cardiovascular Diseases; Female; Humans; Inflammation; Isoenzymes; Male; Middle Aged; Myocardial Infarction; Risk Factors; Tartrate-Resistant Acid Phosphatase; Young Adult

Myocardial infarction is one of the most common manifestations of cardiovascular disease. In the present study, we investigated the protective effect of betaine, a potent lipotropic molecule, on changes in the levels of lysosomal enzymes and lipid peroxidation in isoprenaline-induced myocardial infarction in Wistar rats, an animal model of myocardial infarction in man. Male albino Wistar rats were pretreated with betaine (250 mg/kg body weight) daily for a period of 30 days. After the treatment period, isoprenaline (11 mg/100 g body weight) was intraperitoneally administered to rats at intervals of 24 h for 2 days. The activities of lysosomal enzymes (beta-glucuronidase, beta-galactosidase, beta-glucosidase, and acid phosphatase) were significantly (p < 0.05) increased in plasma with a concomitant decline in the activities of these enzymes in heart tissue of isoprenaline-administered rats. Also, the level of lipid peroxidation was higher in heart lysosomes of isoprenaline-injected rats. Pretreatment with betaine daily for a period of 30 days to isoprenaline-induced rats prevented the changes in the activities of these lysosomal enzymes. Oral treatment with betaine (250 mg/kg body weight) to normal control rats did not show any significant effect in all the biochemical parameters studied. Thus, the results of our study show that betaine protects the lysosomal membrane against isoprenaline-induced myocardial infarction. The observed effects might be due to the free radical-scavenging and membrane-stabilizing properties of betaine.

Topics: Acid Phosphatase; Animals; Betaine; Cardiotonic Agents; Enzyme Activation; Glycoside Hydrolases; Heart; Isoproterenol; Lipid Peroxidation; Lipotropic Agents; Lysosomes; Male; Myocardial Infarction; Rats

Coronary heart disease (CHD) is a major killer worldwide. Atherosclerosis, which is the basis of CHD, is believed to be an inflammatory disorder. Though various aspects of atherosclerosis are extensively studied, leukocytic hydrolytic enzymes are not studied very well with respect to CHD.. This study was planned to assess changes associated with leukocytic hydrolases in CHD patients.. A tertiary care hospital; case-control study.. 106 patients with acute myocardial infarction, 60 patients with unstable angina and 45 healthy controls were included in the study. Acid phosphatase, lysozyme, adenosine deaminase (ADA) and cathepsin-G levels were estimated from leukocytes. Reduced glutathione (GSH) and malondialdehyde (MDA) levels were measured.. Statistical comparison of data was done using student's t-test (unpaired). Correlation difference was calculated by using Pearson correlation coefficient.. Significantly higher levels of acid phosphatase, lysozyme, ADA with lower levels of cathepsin G in leukocytes were observed in CHD group. We also found significantly higher levels of serum MDA with lower concentrations of blood GSH in CHD group. In diabetic CHD group, significantly higher levels of leukocytic acid phosphatase, lysozyme, ADA and serum MDA with lower levels of cathepsin G and blood GSH were observed.. Our study indicates that leukocyte hydrolytic enzymes, mainly acid phosphatase, lysozyme and ADA were more active in CHD patients and may contribute to inflammation related with CHD. Its also indicates that leukocyte cathepsin-G may have antiinflammatory role.

Topics: Acid Phosphatase; Acute Disease; Adult; Angina, Unstable; Cathepsin G; Cathepsins; Coronary Disease; Female; Humans; Leukocytes; Male; Malondialdehyde; Middle Aged; Muramidase; Myocardial Infarction; Serine Endopeptidases

Topics: Acid Phosphatase; Aged; Biomarkers; Humans; Male; Myocardial Infarction; Prostate-Specific Antigen; Protein Tyrosine Phosphatases; Shock, Cardiogenic

Cardiac and plasma activities of marker lysosomal enzymes were studied in Wistar rats with metabolic (epinephrine) and occlusion (ligation of coronary arteries) myocardial infarction. Activity of all examined lysosomal enzymes significantly increased in the myocardium and blood plasma starting from the first day after ligation of the coronary arteries and was accompanied by leukocytic infiltration of the myocardium. Enzyme activity gradually decreased to postoperation day 14. In metabolic infarction leukocytic infiltration and specific activity of lysosomal enzymes rose gradually and attained maximum to postoperation day 14, while the signs of labilization of lysosomal membranes appeared from the first postoperation day. Plasma activity of lysosomal enzymes in metabolic infarction increased smoothly and peaked on day 14.

Topics: Acid Phosphatase; Animals; beta-Galactosidase; Cathepsin D; Coronary Vessels; Deoxyribonucleases; Hydrolases; Ligation; Lysosomes; Male; Myocardial Infarction; Myocardium; Norepinephrine; Rats; Rats, Wistar; Vasoconstrictor Agents

Isoproterenol was used as a drug which, when administered in high doses, is able to induce lysosomal enzyme activity changes in in vivo conditions. We correlated lysosomal enzyme activity in the absence and presence of isoproterenol, obtained in whole animals and in HeLa and HepG2 cells in tissue culture. In vivo experiments: male Wistar rats (270-300 g) were treated subcutaneously with isoproterenol in various doses. Effect of isoproterenol on lysosomal enzyme activity was assayed in the heart after differential centrifugation. In vitro experiments: Isoproterenol in concentrations 0.1-100 microg/ml was added to HeLa and HepG2 cells and the activity of lysosomal enzyme was measured in the cell homogenate. In the sedimentable and nonsedimentable fractions of the rat myocardium, the isoproterenol-induced changes in the activity of lysosomal enzyme were time-and dose-dependent. In HeLa cells, isoproterenol administration caused a dose-dependent increase of lysosomal enzyme activity, while in HepG2 cells the activity remained unchanged. Thus the isoproterenol-induced changes in lysosomal enzyme activity in the rat myocardium were comparable with the results found in vitro in HeLa cells.

Topics: Acetylglucosaminidase; Acid Phosphatase; Animals; Carcinoma, Hepatocellular; Cathepsin D; Glucuronidase; Heart; HeLa Cells; Humans; Isoproterenol; Kinetics; Liver Neoplasms; Lysosomes; Male; Myocardial Infarction; Myocardium; Rats; Rats, Wistar; Tumor Cells, Cultured

The electrocardiogram (ECG) was recorded and the serum levels of creatine kinase (CK), aspartate transaminase (ASAT) and prostatic acid phosphatase (PAP) was measured in 22 patients undergoing transurethral resection of the prostate (TURP) under spinal or epidural anaesthesia. The irrigating fluid consisted of 1.5% glycine and 1% ethanol, and absorption of the fluid was monitored by detection of alcohol in the expired breath. The results show that nine of the 11 patients (82%) who absorbed more than 1,000 ml of irrigating fluid had developed ECG changes 24 h after the operations. The most common alteration was depression of the T wave. This sign was only seen in one (9%) of the patients who absorbed none or very small amounts of irrigating fluid (P < 0.001). The serum activity of CK and ASAT increased in five patients who also developed ECG changes, and the highest values were recorded 24 h after TURP. The CK-MB isoenzyme was detected in 85% of the samples with elevated total CK, but the criteria for myocardial infarction were never fulfilled. In contrast, PAP increased in all patients and the highest level occurred at the end of TURP. The activity-time profiles suggest that CK and ASAT entered the circulation by a mechanism different from that of PAP. We conclude that absorption of glycine solution during TURP is frequently followed by nonspecific ECG signs of altered cardiac function and also that the serum activities of CK and ASAT increase in some of these patients.

Topics: Absorption; Acid Phosphatase; Aged; Aged, 80 and over; Anesthesia, Epidural; Anesthesia, Spinal; Aspartate Aminotransferases; Creatine Kinase; Electrocardiography; Ethanol; Glycine; Humans; Isoenzymes; Male; Middle Aged; Myocardial Infarction; Myocardium; Potassium; Prospective Studies; Prostate; Prostatectomy; Sodium; Therapeutic Irrigation

In isoprenaline-induced myocardial infarction in rabbits, the circulating neutrophils (neu) were in an activated state. tanshinone (tan, ig) suppressed the neu functions (acid-phosphatase release, adhesiveness, and phagocytosis) dose-dependently and reduced myocardial necrosis concomitantly. There was a positive correlation between neu functions and myocardial necrosis. In addition, tan caused an obvious decrease in content of lipoperoxide malondialdehyde in serum and myocardium, an increase in superoxide dismutase activity, an inhibition of leukocytic infiltration, and a production of prostaglandin E2 in myocardium. These effects were also related closely to the suppression of neu functions. Anti-inflammatory drug dexamethasone was used as control and had similar effects on Neu functions and myocardial infarction. It is suggested that the prophylactic effects of tan on myocardial infarction may result from the inhibition of circulating neu functions.

Topics: Abietanes; Acid Phosphatase; Adhesiveness; Animals; Dose-Response Relationship, Drug; Female; Male; Myocardial Infarction; Myocardium; Neutrophils; Phagocytosis; Phenanthrenes; Rabbits

Cytochemical assays of neutrophil acid phosphatase, beta-glucuronidase, N-acetyl-beta-D-glycosamidase (NAG), myeloperoxidase activities, and the Sudan black B test, were carried out in 25 patients with myocardial infarction. Leucocytosis seen in the early days of infarction was associated with increased proportion of neutrophils characterized by high activities of the enzymes in question and enhanced reaction with Sudan black B. Neutrophilosis of the early myocardial infarction may result from the activity of the marginal cell fraction. The fact that increased myeloperoxidase activity and the enhanced response to Sudan black B persist through 14 days of the disease, coupled with a rise in neutrophil NAG activity on day 14, expands possibilities of myocardial infarction diagnosis.

Topics: Acetylglucosaminidase; Acid Phosphatase; Adult; Female; Glucuronidase; Histocytochemistry; Humans; Leukocyte Count; Male; Middle Aged; Myocardial Infarction; Neutrophils; Peroxidase

The activity of some organ specific enzymes of the liver subcellular structures in the blood serum was examined in 56 patients with cardiogenic shock. The correlation between the gravity of clinical signs of cardiogenic shock and blood enzyme degree was revealed. It was concluded that biochemical criteria could be used in the diagnosis of irreversible changes in the liver in cardiogenic shock.

Topics: Acid Phosphatase; Aged; Cholinesterases; Female; Fructose-Bisphosphate Aldolase; Glutamate Dehydrogenase; Humans; Liver; Male; Middle Aged; Myocardial Infarction; Organ Specificity; Shock, Cardiogenic

Topics: Acetylglucosaminidase; Acid Phosphatase; Adult; Azo Compounds; Female; Glucuronidase; Humans; Male; Middle Aged; Myocardial Infarction; Naphthalenes; Neutrophils; Peroxidase

Topics: Acid Phosphatase; Adult; Aged; alpha-Tocopherol; Cholinesterases; Female; Fructose-Bisphosphate Aldolase; Glutamate Dehydrogenase; Humans; Lipid Peroxides; Liver; Male; Middle Aged; Myocardial Infarction; Organ Specificity; Tocopherols; Vitamin E

Leucocytic acid phosphatase (AP) activity was measured cytochemically in 21 myocardial-infarction patients aged 37 to 57. Neutrophil leucocytosis was found to result from an increase in the quantity of cells with high activity of the enzyme. Neutrophil AP activity was elevated during the first days of the infarction and dropped to the baseline level on day 14. Between days 7 and 14, the numbers of lymphocytes with cytoplasmatic AP localization were reduced, suggesting lysosome stabilization at this stage of myocardial infarction.

Topics: Acid Phosphatase; Adolescent; Adult; Female; Humans; Leukocytes; Lymphocytes; Lysosomes; Male; Middle Aged; Myocardial Infarction; Neutrophils; Time Factors

A rapid radioassay was used to characterise the adenosine diphosphatase (ADPase) activities in human plasma. There was a major peak at pH 9.3, 80% of whose activity was attributable to non-specific alkaline phosphatase, with the remaining 20% probably due to a specific ADPase. There was also a small peak of ADPase activity at pH 4.0. Inhibitor and chromatographic studies showed that whilst much of this activity was attributable to non-specific acid phosphatase, there was a discrete acid ADPase. Assays of plasma ADPase activities in vascular disorders, including myocardial infarction, peripheral vascular disease and diabetes mellitus, reveal no alterations from control values. Activities of alkaline ADPase were elevated in both chronic and acute liver failure. Acid ADPase was also increased in chronic liver disease and it is suggested that alterations in ADPase activities in liver disorders may contribute to the haemostatic problems observed in these patients.

Topics: Acid Phosphatase; Acute Disease; Alkaline Phosphatase; Apyrase; Chromatography, Gel; Chronic Disease; Humans; Hydrogen-Ion Concentration; Kinetics; Liver Diseases; Myocardial Infarction; Phosphoric Monoester Hydrolases; Vascular Diseases

Topics: Acid Phosphatase; Adult; Enzyme Activation; Female; Humans; Lymphocytes; Male; Middle Aged; Myocardial Infarction; Neutrophils; Time Factors

Topics: Acid Phosphatase; Animals; Cholesterol; Coronary Vessels; Dietary Fats; Lipids; Macrophages; Male; Myocardial Infarction; Myocardium; Rats; Sarcoplasmic Reticulum; Succinate Dehydrogenase; Triglycerides

Twenty-two cat hearts were perfused according to Langendorff technique and myocardial regional ischemia was induced by occlusion of left anterior coronary artery. Separation of particulate (bound) from soluble (free) fraction, and subsequent fractionation into plasma membranes, lysosomes, sarcoplasmic reticulum, and mitochondria were performed by sucrose density gradient ultracentrifugation. By ischemia for 60 min, particle-bound activity of cathepsin D decreased from 4.2 +/- 0.24 U/mg protein to 3.2 +/- 0.31 U/mg protein (p less than 0.01). Likewise, the particle-bound activity of beta-glucuronidase decreased from 11.9 +/- 0.92 U/mg protein to 6.2 +/- 1.28 U/mg protein (p less than 0.01). Accordingly, free/bound activity ratios of cathepsin D increased from 0.8 to 1.9 and beta-glucuronidase from 0.9 to 2.8, respectively. Conspicuous fall from 12.8 +/- 0.6 U/mg protein to 8.0 +/- 0.97 U/mg protein (p less than 0.01) in absolute specific activity of cathepsin D bound to the lysosomal fraction, presents definitive evidence of lysosomal release of the acid hydrolases during the early phase of myocardial ischemia. Electron microscopic observation of the ischemic myocytes revealed ultrastructural alterations of the lysosomes suggestive of autophagic degradation of various subcellular organelles.

Topics: Acid Phosphatase; Animals; Cathepsins; Cats; Female; Glucuronidase; Hydrolases; Lysosomes; Male; Myocardial Infarction; Myocardium; Protein Binding; Subcellular Fractions

The results of histochemical, histoenzymological, and fluorescence microscopy studies of the conductive tissue of the heart in acute myocardial infarction in 30 fatal cases are presented. Focal decrease in redox and hydrolytic enzymes, monoaminoxidase, and cholinesterase in elementa of the conduction system as well as changes in the pattern of fluorescence of the specific muscle cells were found. The intensity of metabolic lesions was more pronounced at early stages of myocardial infarction in those cases where the conducting pathways were proximal to the foci of necrosis.

Topics: Acid Phosphatase; Acute Disease; Aged; Alkaline Phosphatase; Cholinesterases; Cytochromes; Electron Transport Complex IV; Glutamate Dehydrogenase; Glutamates; Glycerolphosphate Dehydrogenase; Glycerophosphates; Heart Conduction System; Humans; L-Lactate Dehydrogenase; Lactates; Malate Dehydrogenase; Malates; Middle Aged; Monoamine Oxidase; Myocardial Infarction; NADPH Dehydrogenase; Succinate Dehydrogenase; Succinates

The spectrum of acid phosphatase isoenzymes was studied by means of disk electrophoresis in polyacrylamide gel. Seven isofractions were detected of this enzyme in blood plasma. In patients with the acute stage of myocardial infarction the amount of isofraction 3 was increased, its electrophoretic mobility was 0.479 +/- 0.059. It is suggested to use the test for acid phosphatase fraction 3 in blood plasma as an auxiliary method in the diagnosis of pathological conditions of the myocardium.

Topics: Acid Phosphatase; Acute Disease; Adult; Aged; Clinical Enzyme Tests; Female; Humans; Isoenzymes; Male; Middle Aged; Myocardial Infarction; Reference Values; Time Factors

The morpho-functional features of peripheral blood leukocytes were studied in 50 rabbits with experimental myocardial infarction at various intervals after ligation of the anterior interventricle artery. Changes in the leukocytes were compared with the morphological picture of myocardial infarction. In the acute period of experimental myocardial infarction not only quantitative changes were found to occur but also functional values of leukocytes changes: the content of glycogen and the activities of peroxidase and phagocytic activity of granulocytes were reduced, while the activity of alkaline phosphatase increased. Electron microscopic examinations of lymphocytes revealed ultrastructural changes in mitochondria. In the subacute period of the disease some of the values showed a trend for normalization. In the period of recuperation when the zone of infarction in rabbits is replaced by crude fiber connective tissue all the values under study in the peripheral blood became normal. The exceptions were the animals with extensive as well as complicated myocardial infarctions.

Topics: Acid Phosphatase; Acute Disease; Animals; Glycogen; Granulocytes; Leukocytes; Mitochondria, Heart; Myocardial Infarction; Peroxidases; Phagocytosis; Rabbits

Topics: Acid Phosphatase; Adult; Aged; Animals; Cathepsins; Clinical Enzyme Tests; Dogs; Humans; Middle Aged; Myocardial Infarction; Myocardium; Ribonucleases

Topics: Acid Phosphatase; Acute Disease; Alkaline Phosphatase; Fatty Acids, Nonesterified; Humans; Male; Middle Aged; Myocardial Infarction

To evaluate lysosomal involvement in myocardial infarction, coronary artery thrombosis was induced by ligation in 16 dogs. Biopsies of infarcted and normal left ventricles were studied by ultrastructural cytochemistry and subcellular fractionation (0.25 M sucrose) from 30 min to 96 hrs post injury. Normal myocardium contained few "classical" (residual body) lysosomes: instead, acid phosphatase and aryl sulfatase were localized to longitudinal and to lateral sac elements of the sarcoplasmic reticulum. In postnuclear (450 X gm, 10 min) supernates, lysosomal acid phosphatase and beta-glucuronidase were divided 60:40 between sedimentable (98,000 X gm, 15 min) and non-sedimentable fractions of normal endocardium and epicardium (studied separately). At 2 hrs post infarction, ischemic muscle showed: 1) loss of membrane-bound acid phosphatase and aryl sulfatase; 2) mitochondrial damage; 3) loss of glycogen and disappearance of I but not A bands; and 4) entry into cells of colloidal lanthanum (= loss of plasma membrane integrity. Total lysosomal hydrolase did not increase until 6-5 hrs post infarct. At 2 hrs, significant increments (32 +/- 7%) were found in nonsedimentable acid phosphatase and beta-glucuronidase of endocardium (P less than 0.005 vs. normal) but the epicardium. In dogs given methylprednisolone (50 mg/k) 30 min post infarct, ultrastructural cytochemistry showed retention of lysosomal enzymes within endocardial sarcoplasmic reticulum and no significant redistribution of enzymes into non-sedimentable fractions (vs. eight paired, infarcted, untreated controls). Data show early disruption of lysosomes in myocardial infarction and their protection by steroid given after the acute insult.

Topics: Acid Phosphatase; Animals; Arylsulfatases; Dogs; Glucuronidase; Histocytochemistry; Lysosomes; Methylprednisolone; Myocardial Infarction; Myocardium; Sarcolemma; Sarcoplasmic Reticulum

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Carboxylic Acids; Dogs; Esterases; Fluoresceins; Isoenzymes; L-Lactate Dehydrogenase; Ligation; Malate Dehydrogenase; Mercury; Myocardial Infarction; Organomercury Compounds

The effect of ischemia on the integrity of myocardial lysosomes was observed 3 1/2 and 24 hours after the production of infarcts in 20 anesthetized closed-chest dogs by electrically induced thrombosis of the left anterior descending coronary artery. Biopsies from normal, marginal and infarcted areas were fixed and incubated to localize the lysosomal enzymes acid phosphatase and aryl sulphatase. Reaction product in normal cells was localized in small circular or oblong profiles between bundles of myofilaments and adjacent to mitochondria. In addition, curvilinear, membrane-bound profiles containing reaction product were found in close apposition to transverse tubules and near the free margins of the myocardial cells. Thus the distribution of elements of the sarcoplasmic reticulum. Additional reaction product was also seen in residual bodies, on myelin figures, and in the few conventional appearing spherical lysosomes. Little or no acid phosphatase or aryl sulphatase reaction product was seen in the sarcoplasmic reticulum of infarcted myocardium. The degree of cellular degeneration correlated with disappearance of enzyme activity from the sarcoplasmic reticulum and included disruption of membranes and loss of mitochondrial matrix and erosion of I but not A bands. Marginal areas showed variable amounts of cellular degeneration. Separation of myofilament bundles and loss of glycogen correlated with the localized disappearance of acid phosphatase and aryl sulphatase activity in marginal tissue. Disruption of mitochondrial and erosion of I bands correlated with extensive loss of these enzymes. The data suggest that degeneration of myocardial cells following ischemic injury is associated with release of endogenous lysosomal enzymes from the sarcoplasmic reticulum.

Topics: Acid Phosphatase; Animals; Arylsulfonates; Dogs; Glycogen; Histocytochemistry; Lysosomes; Microscopy, Electron; Mitochondria, Muscle; Myocardial Infarction; Myocardium; Myofibrils; Sarcoplasmic Reticulum

Topics: Acid Phosphatase; Animals; Clinical Enzyme Tests; Coronary Vessels; Dogs; Enzymes; Glucuronidase; Hexosaminidases; Lysosomes; Myocardial Infarction

Topics: Acid Phosphatase; Acute Disease; Adult; Aged; Alkaline Phosphatase; Angina Pectoris; Aspartate Aminotransferases; Butyrates; Carbonic Anhydrases; Catalase; Ceruloplasmin; Cholinesterases; Clinical Enzyme Tests; Coronary Disease; Female; Humans; Male; Middle Aged; Myocardial Infarction

Topics: Acid Phosphatase; Alkaline Phosphatase; Aminopeptidases; Animals; Dihydrolipoamide Dehydrogenase; Esterases; Heart; Inosine; L-Lactate Dehydrogenase; Male; Microscopy, Electron; Mitochondria, Muscle; Myocardial Infarction; Myocardium; NAD; Nandrolone; Orotic Acid; Rabbits; Succinate Dehydrogenase; Vitamin B 12

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Biological Transport; Blood Proteins; Coronary Vessels; Creatine Kinase; Dogs; Isoenzymes; L-Lactate Dehydrogenase; Ligation; Lymph; Malate Dehydrogenase; Myocardial Infarction; Potassium; Time Factors

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Dogs; Glutamate Dehydrogenase; Isocitrate Dehydrogenase; Isoenzymes; L-Lactate Dehydrogenase; Lymph; Malate Dehydrogenase; Methods; Mitochondria; Myocardial Infarction; Myocardium; Pulmonary Artery

Topics: Acid Phosphatase; Animals; Dogs; Hydrocortisone; Lymph; Lysosomes; Myocardial Infarction; Myocardium

Topics: Acid Phosphatase; Alkaline Phosphatase; Amylases; Biliary Tract Diseases; Bone Diseases; Clinical Enzyme Tests; Creatine Kinase; Enzymes; Humans; Isoenzymes; Liver Diseases; Male; Muscular Diseases; Myocardial Infarction; Nervous System Diseases; Organ Specificity; Oxidoreductases; Pancreatic Diseases; Prostatic Diseases; Pulmonary Embolism; Transaminases

Topics: Acid Phosphatase; Adenosine Diphosphate; Adenosine Triphosphate; Anabolic Agents; Animals; Disease Models, Animal; Dogs; Glucuronidase; Heart; Heart Ventricles; Lactates; Myocardial Contraction; Myocardial Infarction; Myocardium; Norepinephrine; Phosphocreatine; Proline; Pyruvates; Time Factors

Topics: Acid Phosphatase; Animals; Coronary Disease; Coronary Vessels; Dogs; Female; Glucuronidase; Glycogen; Heart Ventricles; In Vitro Techniques; Ligation; Lysosomes; Male; Muscles; Myocardial Infarction; Papillary Muscles; Potassium; Time Factors

Topics: Acid Phosphatase; Animals; Coronary Vessels; Dogs; Female; Glycogen; Hydrogen-Ion Concentration; In Vitro Techniques; Ischemia; Ligation; Lysosomes; Male; Muscles; Myocardial Infarction; Papillary Muscles; Potassium; Time Factors

Topics: Acid Phosphatase; Animals; Dihydrolipoamide Dehydrogenase; Dogs; Electrocardiography; Glucosephosphate Dehydrogenase; Glutamate Dehydrogenase; Glycerolphosphate Dehydrogenase; L-Lactate Dehydrogenase; Malate Dehydrogenase; Male; Methandrostenolone; Myocardial Infarction; Myocardium; Oxidoreductases; RNA; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adolescent; Adult; Alkaline Phosphatase; Anemia; Animals; Bacterial Infections; Blood Cell Count; Cerebrovascular Disorders; Female; Gastroenteritis; Histocytochemistry; Humans; Male; Middle Aged; Myocardial Infarction; Neoplasms; Neutrophils; Rabbits; Virus Diseases

Topics: Acid Phosphatase; Animals; Dihydrolipoamide Dehydrogenase; Dogs; Glucosephosphate Dehydrogenase; Glutamate Dehydrogenase; Histocytochemistry; L-Lactate Dehydrogenase; Malate Dehydrogenase; Myocardial Infarction; Myocardium; Oxidoreductases; Regeneration; RNA; Succinate Dehydrogenase

Topics: Acid Phosphatase; Alkaline Phosphatase; Blood Group Incompatibility; Female; Humans; Infant, Newborn; Myocardial Infarction; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Complications, Cardiovascular; Pregnancy, Prolonged; Rh-Hr Blood-Group System

Topics: Acid Phosphatase; Alkaline Phosphatase; Capillaries; Coronary Disease; Coronary Vessels; Dihydrolipoamide Dehydrogenase; Electron Transport Complex IV; Esterases; Glycogen; Heart Conduction System; Heart Neoplasms; Histocytochemistry; Humans; Hypertension; Lipase; Methods; Myocardial Infarction; NAD; NADP; Regional Blood Flow; Succinate Dehydrogenase

Topics: Acid Phosphatase; Alkaline Phosphatase; Clinical Enzyme Tests; Creatine Kinase; Enzymes; Female; Humans; Isoenzymes; Liver Diseases; Male; Metabolism, Inborn Errors; Muscular Diseases; Myocardial Infarction; Transaminases

Topics: Acid Phosphatase; Animals; Deoxyribonucleases; Dogs; Glucuronidase; Lysosomes; Myocardial Infarction; Myocardium; Peptide Hydrolases

Topics: Acid Phosphatase; Acute Disease; Adolescent; Adult; Aged; Female; Histocytochemistry; Humans; Male; Middle Aged; Myocardial Infarction; Neutrophils; Pneumonia; Tuberculosis, Pulmonary

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Dogs; Electron Transport Complex IV; Esterases; Histocytochemistry; Lipase; Methods; Myocardial Infarction; Myocardium; NAD; NADP; Oxidation-Reduction; Succinate Dehydrogenase; Time Factors

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Dogs; Male; Myocardial Infarction; Myocardium; Potassium

Topics: Acid Phosphatase; Acute Disease; Age Factors; Alkaline Phosphatase; Animals; Avitaminosis; Bone Neoplasms; Carcinoma; Chronic Disease; Diabetes Mellitus; Esophageal Neoplasms; Estrus; Female; Hematologic Diseases; Hemoglobinuria, Paroxysmal; Histocytochemistry; Hodgkin Disease; Humans; Infections; Leukemia; Leukocytes; Liver Diseases; Lung Neoplasms; Male; Myocardial Infarction; Neutrophils; Pregnancy; Prostatic Neoplasms; Radiation Injuries; Stress, Physiological

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Aspartate Aminotransferases; Clinical Enzyme Tests; Humans; Hydroxybutyrate Dehydrogenase; L-Lactate Dehydrogenase; Male; Myocardial Infarction; Phenylalanine

Topics: Acid Phosphatase; Adult; Aged; Angina Pectoris; Female; Humans; Male; Middle Aged; Myocardial Infarction

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Arteries; Coronary Vessels; Electron Transport Complex IV; Esterases; Glucosyltransferases; Histocytochemistry; Myocardial Infarction; Myofibrils; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Esterases; Female; L-Lactate Dehydrogenase; Myocardial Infarction; Myocardium; Rats

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Amylases; Aspartate Aminotransferases; Clinical Enzyme Tests; Creatine Kinase; D-Alanine Transaminase; Diagnosis, Differential; Humans; Liver Diseases; Muscular Diseases; Myocardial Infarction; Pancreatitis

Ten consecutive cases of acute transmural myocardial infarction were accompanied by a rise of 50 to 400 percent in the serum acid phenylphosphatase. The increase in phosphatase began several hours after onset of symptoms and lasted 3 to 5 days. A similar rise was seen during the acute stages of other thromboembolic diseases. While the mechanism by which this acid hyperphenylphosphatasia occurs is not clear, platelets may play an important role.

Topics: Acid Phosphatase; Acute Disease; Alanine Transaminase; Aspartate Aminotransferases; Blood; Clinical Enzyme Tests; Humans; Myocardial Infarction

Topics: Acid Phosphatase; Aspartate Aminotransferases; Cardiovascular Diseases; Clinical Enzyme Tests; Fructose-Bisphosphate Aldolase; Humans; Isoenzymes; L-Lactate Dehydrogenase; Malate Dehydrogenase; Myocardial Infarction; Succinate Dehydrogenase