muramidase and Vascular-Diseases

Topics: Animals; Avitaminosis; Bronchoscopy; Burns; Central Nervous System Diseases; Chick Embryo; Child; Crystallization; Ear Diseases; Eye Diseases; Female; Gastrointestinal Diseases; Genital Diseases, Female; Humans; Liver Diseases; Mouth Diseases; Muramidase; Nose Diseases; Postoperative Complications; Respiratory Tract Diseases; Typhus, Epidemic Louse-Borne; Vascular Diseases; Wounds and Injuries

Topics: Blood Cells; Cholinesterase Inhibitors; Contrast Media; Drug Hypersensitivity; Glucuronidase; Humans; Hypertonic Solutions; Muramidase; Nervous System Diseases; Protein Binding; Serum Albumin; Vascular Diseases; Water-Electrolyte Balance

Progression rate of disease processes in smoke-induced lung injuries varies greatly. Diverse pathophysiological mechanisms may trigger these divergences. The aim of this study was to evaluate whether circulating markers of monocytes/macrophages and/or neutrophil [i.e. lysozyme (LZM) or myeloperoxidase (MPO)] were associated with reduced values of diffusion capacity (DL,CO), which is considered to serve as a mirror of pulmonary microvascular derangement and an early sign of tissue remodelling in smokers. Data obtained from 134 smokers (GOLD stage ≤1) and 24 matched healthy non-smoking volunteers were evaluated in a cross-sectional study design. Lung function tests as well as single breath test of DL,CO were assessed according to ATS/ERS guidelines. Biomarkers were measured in serum by means of sensitive immunoassays. A subgroup of smokers with normal lung function was created to minimize confounding, by excluding datasets showing significant airflow limitation and abnormally high values of carboxy haemoglobin (COHb), the latter indicating recent smoking. The capacity of serum lysozyme to correctly identify abnormally low values of DL,CO (i.e. <1·9SD units), tended to be higher than that of Myeloperoxidase as assessed by analyses of receiver operated curves (ROC; AUC 0·81, 95%CI: 0·69-0·89 versus AUC 0·67, 95%CI: 0·60-0·81). It is concluded that serum levels of lysozyme, reflecting mainly activated monocytes/macrophages but also neutrophils, were significantly associated with isolated decrements of DL,CO in smokers with normal lung function tests. This suggests monocytes/macrophages to have a significant mechanistic role in early phases of the disease process and/or pulmonary microvascular damage.

Topics: Adult; Aged; Area Under Curve; Biomarkers; Case-Control Studies; Chi-Square Distribution; Cross-Sectional Studies; Female; Humans; Lung; Macrophages; Male; Microvessels; Middle Aged; Monocytes; Muramidase; Neutrophils; Peroxidase; Predictive Value of Tests; Prognosis; Pulmonary Diffusing Capacity; ROC Curve; Smoking; Up-Regulation; Vascular Diseases

Defibrotide (DEF) is a polydeoxyribonucleotide agent provided with profibrinolytic and antithrombotic properties. Moreover, an antiischemic, cardioprotective effect of the drug has recently been demonstrated in experimental animals. Increasing evidence exists of the important role played by neutrophils in the development of tissue damage during chronic and acute ischemia and in the early phases of reperfusion. In order to evaluate whether the overall cytoprotective effect of DEF could be based, at least in part, on a neutrophil-involving mechanism, the authors studied the in vitro effects of the drug on human neutrophil activation triggered by several specific stimuli. The drug dose-dependently (10-100 microM) inhibited enzyme release, superoxide anion generation, and chemiluminescence induced in neutrophils by the chemoattractant oligopeptide fMLP and by the divalent cation ionophores A23187 and ionomycin. The increase of extracellular calcium concentration from 0.5 to 2.0 mM antagonized the inhibitory effect of DEF. The use of the fluorescent probe Fura 2/AM led them to show that DEF is able to reduce the cytosolic free calcium increase following specific stimulation by affecting extracellular calcium entrance. Such a behavior resembles that of calcium-antagonistic drugs, thus suggesting that DEF works, at least in part, similarly to calcium entry blockers. Such an activity on cell calcium translocation could represent the underlying molecular mechanism of cytoprotection. Finally, the inhibitory action on neutrophil functions may play a role in tissue protection during ischemic injury.

Topics: Calcium; Dose-Response Relationship, Drug; Fibrinolytic Agents; Free Radicals; Humans; Luminescent Measurements; Muramidase; Neutrophils; Polydeoxyribonucleotides; Superoxides; Vascular Diseases

We have examined sixty-seven surgically removed allograft kidneys to identify the different leukocyte subsets of interstitial infiltration and the early vascular lesions which characterize renal allograft rejection. Histochemical and immunohistochemical results (mouse monoclonal antibodies anti: Leu 1, Leu 3a-3b, Leu 7, Leu 2a, OK Ia-Dr, OKB2, Leu M1, Leu M3; rabbit heteroclonal antibodies anti -: IgA, IgG, IgM, C3, fibrinogen, lysozyme; lectins-ABC: RCA, WGA, UEA) and routine histochemical staining have shown an increase of T-helper and T-activated lymphocyte subsets in acute rejection. Neutrophilic leucocytes were present in hyperacute rejection; macrophages were also noted. In chronic rejection, several lymphocyte subsets, in different ratios, were identified. Monocyte/macrophage leukocytes were the most abundant cell population. IgA deposits were noted on tubular epithelia in hyperacute and chronic rejections. IgM deposits were observed in vascular walls in chronic rejection. C3 and fibrinogen deposits were seen in glomerular capillaries and in arterial walls, although in different ratios, in all cases of renal allograft rejections. We have generally seen weak reactions to IgG deposits. Histochemical analysis of lectin receptors has given different results according to the type of rejection considered. In hyperacute rejection, receptors for WGA were found both on glomerular endothelial cells and on the tubular brush border. In the latter, receptors for RCA were also found. In acute rejection, receptors for UEA and WGA were found in a lower number of cases of acute vascular rejection. In acute cellular rejection, receptors for RCA, UEA and WGA were recognized in tubular epithelia. In acute vascular rejection, as well as in chronic rejection, only receptors for WGA were present on tubular epithelia and on capillary loop endothelium. The use of anti-human lysozyme antibodies has yielded the following results: in acute and hyperacute rejection, when renal failure occurred, we saw a high ratio of lysozyme, either coarsely granular or diffuse in the proximal tubular epithelia. Lysozyme was found in myelocyte/macrophage cells within capillary loops and arterial walls, when acute necrotizing vasculitis was present. In acute rejection, proximal tubular cells were lysozyme-negative or lysozyme-positive only segmentally, especially when obliterative vasculitis by fibrointimal proliferation was present and renal function progressively failed. In most of the chron

Topics: Acute Disease; Graft Rejection; Humans; Immunoglobulins; Inflammation; Kidney; Kidney Transplantation; Lectins; Lymphocytes; Muramidase; Plant Lectins; Receptors, Mitogen; Staining and Labeling; Vascular Diseases; Wheat Germ Agglutinins

Experimental Rocky Mountain spotted fever was studied in guinea pigs following intraperitoneal inoculation of 10(7) Rickettsia rickettsii. After a 2-day incubation period, animals developed fever, progressive emaciation, and scrotal swelling with necrosis. Vasculitis, with increased small vessel permeability for colloidal carbon, was evident in cremaster muscles as early as 1 day after inoculation. Inflammatory changes in vessels became progressively more severe as numbers of circulating rickettsiae increased. Thrombosis and vascular occlusion were first evident on day 4. Mild thrombocytopenia developed, coinciding with the development of vasculitis, and preceding the appearance of either fibrin-split products in blood or thrombi in vessels. Rickettsiae were first detected in blood on day 2; peak rickettsemia occurred on days 5 to 8. Rickettsiae were demonstrated in inflamed vessels on day 5 and later, but not at earlier stages. Serum lysozyme concentration was moderately elevated and hemolytic complement was moderately depressed throughout the illness. Agglutinating antibody was present in low titers on days 3 to 10. Antibody titers increased on days 12 to 16 after the rickettsiae were cleared from blood. These studies indicate that vasculitis seen early in the course of Rocky Mountain spotted fever is the result of rickettsial infection, but is not dependent on the presence of rickettsiae in endothelial cells or other blood vessel components.

Topics: Agglutination Tests; Animals; Antibodies, Bacterial; Capillary Permeability; Complement System Proteins; Fibrin Fibrinogen Degradation Products; Guinea Pigs; Male; Microscopy, Electron; Muramidase; Muscles; Rickettsia rickettsii; Rocky Mountain Spotted Fever; Testis; Vascular Diseases

Topics: Adolescent; Adult; Aged; Animals; Chronic Disease; Dogs; Female; Glomerular Filtration Rate; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Immunoelectrophoresis; Kidney Diseases; Male; Middle Aged; Muramidase; Myeloma Proteins; Nephritis, Interstitial; Nephrocalcinosis; Nephrotic Syndrome; Pyelonephritis; Rabbits; Vascular Diseases

Topics: Eczema; Gangrene; Granulation Tissue; Humans; Leg Ulcer; Muramidase; Peripheral Vascular Diseases; Pharmacology; Phlebitis; Varicose Ulcer; Vascular Diseases