Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluosol (Alpha Therapeutic Corporation, Los Angeles, CA) an emulsion of perfluorocarbons with a high oxygen-carrying capacity, was approved as an adjunct to alleviate myocardial ischemia during coronary angioplasty. This drug also significantly enhances myocardial salvage presumably related to an action on the neutrophil. The mechanism by which fluosol and its individual components, including the detergent Pluronic F-68, affected neutrophil function was examined. During the incubation of neutrophils with fluosol, a rapid stimulation of superoxide anion production and degranulation which progressively increased over a 30-minute period was detected. Neutrophils incubated with only Pluronic F-68 produced similar amounts of superoxide anion. Cytochalasin B, an inhibitor of phagocytosis, significantly inhibited this superoxide anion generation. As shown previously, neutrophils incubated with fluosol for 30 minutes and then subsequently stimulated manifested a reduction in lysozyme release as compared with untreated cells. Results of an electron microscopic examination confirmed the cellular uptake of the fluosol within phagocytic vacuoles. Neutrophil viability determined by trypan blue was unaffected after fluosol treatment. These observations show that the fluosol emulsion, primarily through micelles formed by the detergent Pluronic F-68, activates human neutrophils by serving as a phagocytic stimulus, which produces a cell refractory to subsequent stimulation.
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PMID:Phagocytic activation of human neutrophils by the detergent component of fluosol. 131 83

Previous studies have demonstrated that intravenous administration of large doses of Fluosol, a perfluorochemical preparation, reduced infarct size 24 h after reperfusion, an effect that was associated with reduced neutrophil infiltration. The effect of a clinically tolerable dose of Fluosol on infarct size after a prolonged period of reperfusion and its mechanism of action on neutrophils remain unknown. Twenty-one anesthesized closed chest dogs were subjected to 90 min of proximal left anterior descending coronary artery occlusion and 72 h of reperfusion. An additional five dogs that did not undergo regional myocardial ischemia were utilized to explore the mechanism of action of Fluosol on neutrophil function. In the infarct study, animals were randomized to receive either intravenous Fluosol (n = 10) or an equivalent volume of Ringer's lactate solution (control; n = 11) at 15 ml/kg body weight during the last 30 min of occlusion and for the 1st 30 min of reperfusion. Fluosol significantly reduced infarct size when expressed as percent area at risk 72 h after reperfusion (13.7 +/- 2.7% vs. 38.3 +/- 4.5%, respectively, p less than 0.001). This reduction was associated with significant improvement in regional wall motion (18.4 +/- 2.3% vs. 5.5 +/- 2%, p less than 0.001). Endocardial blood flow in the ischemic bed was significantly higher 3 h after reperfusion in Fluosol-treated dogs (0.63 +/- 0.08 vs. 0.34 +/- 0.07 ml/min per g, p = 0.01). Reduced capillary plugging by neutrophils with relative preservation of endothelial cell structure was observed in Fluosol-treated animals. Infusion of Fluosol produced a marked transient decrease in peripheral neutrophil and platelet counts in both ischemic and nonischemic dogs and was associated with a significant reduction in total hemolytic complement levels. Studies of neutrophil function ex vivo revealed a reduction in chemotaxis and lysozyme degranulation after infusion of Fluosol. In vitro experiments showed that Fluosol produced a rapid and sustained activation of neutrophils determined by superoxide anion production. These data demonstrate that low dose intravenous Fluosol produces a sustained reduction in infarct size in the canine model. The beneficial effect may be in part due to the suppression of various neutrophil functions in the reperfused myocardium subsequent to peripheral activation by Fluosol. Such interventions may offer a novel therapy to enhance myocardial salvage by sequestration of circulating neutrophils during the critical early reperfusion period.
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PMID:Pharmacologic perturbation of neutrophils by Fluosol results in a sustained reduction in infarct size in the canine model of reperfusion. 172 35

Immune function, T-lymphocyte subsets, serum quantitative immunoglobulin levels, serum lysozyme levels, and circulating immune complex levels were analyzed in patients with idiopathic dilated cardiomyopathy (IDCM). The percentage of helper/inducer T cells (OKT4) was higher and the percentage of suppressor/cytotoxic T cells (OKT8) was lower in IDCM patients than in healthy controls and in patients with ischemic heart disease. IDCM patients, in addition, have higher 5/9+ T cells, a T-cell subset known to give maximal helper activity in B-cell differentiation assays. Peripheral blood mononuclear cells (PBMC) from IDCM patients demonstrated a statistically greater ability to induce B-cell differentiation (helper T-cell function) into plasma cells and a hypofunctioning suppressor T-cell population in an in vitro pokeweed nitrogen (PWN)-driven B-cell differentiation assay. Serum immunoglobulin IgM levels were higher in IDCM patients, but serum lysozyme levels and serum immune complex levels in IDCM patients were normal. These data verify that an immunoregulatory defect exists in IDCM.
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PMID:Immunologic studies of peripheral blood from patients with idiopathic dilated cardiomyopathy. 294 48

During coronary angioplasty, inflation of the balloon within the coronary artery produces transient arterial occlusion and frequently results in myocardial ischemia. Delivery of oxygenated autologous blood to the myocardium at risk during inflation may help mitigate this ischemia. Accordingly, we investigated the feasibility and safety of infusing blood through the central lumen of a dilatation catheter around the guidewire using both a model in vitro and clinical trials. In the tests in vitro, fresh blood was infused at flow rates up to 120 ml/min. Hemolysis was minimal at flow rates of 60 ml/min or less (less than or equal to 0.92 +/- 0.18%), but increased exponentially at higher rates (13.64 +/- 2.37% at 120 ml/min, p less than .002). A similar pattern was observed for potassium release. Platelet and leukocyte counts did not vary significantly, and beta-thromboglobulin and muramidase remained at control levels. Although mean erythrocyte volume did not change, erythrocyte histograms and light microscopy demonstrated a subpopulation of red cell fragments averaging 25 to 40 fl in size at higher rates. A randomized, crossover clinical trial was next performed by delivery of blood perfusion at 60 ml/min to 15 patients undergoing coronary angioplasty. Levels of plasma hemoglobin, beta-thromboglobulin, lactate dehydrogenase, and potassium remained constant before and after the perfusion and the control inflations. The maximum pain score was significantly lower with the perfusion inflation (4.1 +/- 0.8 vs 6.0 +/- 0.9, p less than .003). Relative to baseline, the maximum ST segment elevation during the perfusion inflation (0.5 +/- 0.3 mm) was nearly one-fourth that during the control inflation (1.9 +/- 0.6 mm, p less than .02). Thus, myocardial protection with oxygenated autologous blood perfusion at rates of 60 ml/min appears to be a safe and effective technique that may permit increased inflation time and extend the range of coronary angioplasty to include individuals at high risk for the procedure.
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PMID:Autologous blood perfusion for myocardial protection during coronary angioplasty: a feasibility study. 295 55

A short-lasting hyperthermal stimulus (in a waterbath, until the body temperature reaches 38-38,5 degrees C) caused a drop in mean levels of hemolytic complement (CH50) and its C3 component, and an increase in lysozyme and beta-D-glucuronidase activity in the serum of healthy and IHD-sick subjects, so proving that hyperthermia has an influence of the activity of the complement system and probably labilizing effects on lysosomal membranes.
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PMID:[The effects of a short-lasting hyperthermia on the levels of complement and lysosomal enzymes in the serum of healthy and IHD-sick subjects]. 621 45

Kawasaki disease is an acute vasculitis of unknown cause that occurs predominantly in infants and young children and produces coronary artery aneurysms in approximately 15% to 25% of those affected. In the United States, Kawasaki disease is more commonly the cause of noncongenital heart disease in children than is acute rheumatic fever. Therapy for Kawasaki disease in the acute phase is aimed at reducing inflammation of the coronary artery wall and preventing coronary thrombosis; treatment with high-dose intravenous gamma globulin and aspirin has become the standard of care and reduces the risk of development of coronary artery aneurysms by three- to fivefold. Even when treated with high-dose intravenous immune globulin G (IVIG) regimens within the first 10 days of illness, however, approximately 5% of children with Kawasaki disease develop at least transient coronary artery dilation, and 1% develop giant aneurysms. For those with persistent or recrudescent fever despite initial IVIG infusion, multiple courses of gamma globulin and treatment with cortico- steroids may be indicated. Early experience suggests that therapies aimed at reducing the amount of tumor necrosis factor alpha have a role. For those who develop coronary artery aneurysms, chronic antithrombotic regimens are instituted. When aneurysms are small or moderate in size, aspirin alone may be sufficient, but for patients with giant aneurysms, most experts choose to treat Kawasaki disease with aspirin plus warfarin. Acute coronary thromboses are treated with platelet IIb/IIIa antagonists and thrombolytic therapy. For children with coronary artery stenoses and consequent ischemic heart disease, the therapeutic armamentarium is similar to that used in adults with atherosclerotic coronary artery disease and includes coronary artery bypass grafting and transcatheter interventions.
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PMID:Kawasaki Disease. 1109 28

Disorders of the pericardium are commonly associated with pericardial effusion. Its etiology comprises a broad spectrum of diseases including also malignancies. Pericardiocentesis, pericardioscopy and targeted epicardial biopsy with consecutive pericardial fluid and epicardial biopsy analysis by cytology, molecular biology and immunology establish the underlying etiology in the majority of cases. Of particular therapeutic and prognostic importance is the definite differentiation of malignant pericardial effusion from benign pericardial effusion. Biomarkers for cardiovascular diseases can be divided into biochemical, histological, immunologic, serologic and molecular markers as well as imaging biomarkers. Biomarkers have proven to be useful in the diagnosis, differential diagnosis and prognosis of ischemic heart disease and heart failure. With respect to pericardial disorders, a comprehensive approach combining clinical information, imaging biomarkers, biomarkers of pericardial effusion and analysis of epicardial biopsies often leads to the definite etiologic diagnosis of pericardial effusion. Computed tomography and magnetic resonance imaging allow further characterization of the effusion and, of note, also of the surrounding tissue, which is of particular interest in case of malignancies. Biomarkers of pericardial effusion include biochemical markers, autoantibodies, tumor markers, and cytokines. Analysis of pericardial fluid specific gravity, protein level and lactate dehydrogenase (LDH) separates transudates from exsudates. High adenosine deaminase levels (ADA) and low levels of carcinoembryonic antigen (CEA) in the pericardial effusion are observed in tuberculous pericarditis allowing the differentiation from malignant pericardial effusion. Additional markers, such as interferon and lysozyme, have also been suggested for the diagnosis of tuberculous pericarditis. Tumor markers in pericardial fluid have been used to diagnose malignant pericarditis. CEA levels are significantly higher in malignant than benign effusion. By a cutoff level of CEA > 5 ng/ml the diagnostic sensitivity and specificity are 75% and 100%, respectively, in the diagnosis of malignant pericardial effusion. Further analysis of cytokines and mediators, serologic, immunologic and inflammatory markers may help to understand the pathophysiology of the pericardial disease and provide useful diagnostic information.
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PMID:[Differentiation of malignant from nonmalignant, inflammatory pericardial effusions with biomarkers]. 2002 42