muramidase and Heart-Failure

Heart failure (HF) ensuing myocardial infarction (MI) is characterized by the initiation of a systemic inflammatory response. We aimed to elucidate the impact of myelomonocytic cells and their activation by angiotensin II on vascular endothelial function in a mouse model of HF after MI.. HF was induced in male C57BL/6J mice by permanent ligation of the left anterior descending coronary artery. Compared to sham, HF mice had significantly impaired endothelial function accompanied by enhanced mobilization of Sca-1+c-Kit+ haematopoietic stem cells and Sca-1-c-Kit+ common myeloid and granulocyte-macrophage progenitors in the bone marrow as well as increased vascular infiltration of CD11b+Ly6G-Ly6Chigh monocytes and accumulation of CD11b+ F4/80+ macrophages, assessed by flow cytometry. Using mice with Cre-inducible expression of diphtheria toxin receptor in myeloid cells, we selectively depleted lysozyme M+ myelomonocytic cells for 10 days starting 28 days after MI. While the cardiac phenotype remained unaltered until 38 days post-MI, myeloid cell depletion attenuated vascular accumulation of Nox2+CD45+ cells, endothelial dysfunction, oxidative stress, and vascular expression of adhesion molecules and angiotensin II receptor type 1 (AT1R). Pharmacological blockade of this receptor for 4 weeks did not significantly alter cardiac function, but mimicked the effects of myeloid cell depletion: telmisartan (20 mg/kg/day, fed to C57BL/6J mice) diminished bone marrow myelopoesis and myeloid reactive oxygen species production, attenuated endothelial leucocyte rolling and vascular accumulation of CD11b+Ly6G-Ly6Chigh monocytes and macrophages, resulting in improved vascular function with less abundance of Nox2+CD45+ cells.. Endothelial dysfunction in HF ensuing MI is mediated by inflammatory Nox2+ myeloid cells infiltrating the vessel wall that can be targeted by AT1R blockade.

Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Animals, Genetically Modified; Disease Models, Animal; Endothelial Cells; Heart Failure; Leukocyte Rolling; Macrophages; Male; Mice, Inbred C57BL; Monocytes; Muramidase; Myeloid Cells; Myocardial Infarction; NADPH Oxidase 2; Oxidative Stress; Receptor, Angiotensin, Type 1; Signal Transduction; Telmisartan; Vasculitis

Topics: Adult; Aged; Ascitic Fluid; Female; Heart Failure; Humans; Lung Diseases; Male; Middle Aged; Muramidase; Neoplasms; Pleural Effusion

Topics: Antibodies, Heterophile; Female; Heart Failure; Humans; Isomerism; Lysine; Male; Muramidase

A prospective study was conducted to define the content, significance, and source of lysozyme present in the pleural fluid in human diseases. The pleural fluid lysozyme activity is similar in various malignant and nonmalignant transudates and exudates, and is of limited diagnostic value. The pleural fluid activity correlated well with that of paired serum samples but it had poor correlation with the disease state, the pleural fluid granulocyte counts, and total white blood cell counts. The data suggest that the pleural fluid lysozyme may be derived primarily from the blood and that it is not the product of inflammatory or neoplastic cells in the fluid itself.

Topics: Carcinoma; Female; Granulocytes; Heart Failure; Humans; Leukemia; Liver Cirrhosis; Lung Neoplasms; Lymphoma; Male; Muramidase; Pleural Effusion

On the assumption that increased urinary lysozyme concentration (;lysozymuria') indicates tubular proteinuria and therefore impaired tubular function, urinary lysozyme has been estimated in acute disorders where transient disturbances of renal function might be expected, in cases diagnosed clinically as extrarenal uraemia, and in a few examples of acute renal disease. Reversible lysozymuria occurred with hypokalaemia, postoperative ;collapse', electrolyte depletion, severe extrarenal infection, acute pyelonephritis, the nephrotic syndrome, after a few apparently uncomplicated surgical operations, and very transiently after ventricular fibrillation abolished by DC shock. There was no lysozymuria with severe uraemic heart failure, aspirin and paracetamol poisoning, or severe jaundice, nor in two cases of acute glomerulonephritis. Although lysozymuria may occasionally be useful in the clinical diagnosis of acutely disordered renal function, the results suggest that its value is limited; on the other hand, they have provided information on renal pathophysiology in acute disease.

Topics: Acetaminophen; Acute Disease; Aspirin; Electroshock; Glomerulonephritis; Heart Failure; Humans; Hypokalemia; Jaundice; Kidney; Kidney Diseases; Kidney Failure, Chronic; Kidney Tubules; Muramidase; Myocardial Infarction; Nephrotic Syndrome; Pneumonia; Postoperative Complications; Proteinuria; Pyelonephritis; Uremia; Ventricular Fibrillation

Topics: Alkaline Phosphatase; Autopsy; Bone Marrow Cells; Chromosome Aberrations; Endocarditis; Eosinophilia; Eosinophils; Heart Failure; Humans; Karyotyping; Leukemia; Leukemia, Myeloid; Male; Microscopy, Electron; Middle Aged; Muramidase; Myocardium; Neutrophils; Sex Chromosomes; Vitamin B 12

Topics: Adult; Aged; Asthma; Blood Proteins; Bronchitis; Carbohydrates; Chronic Disease; Diagnosis, Differential; Electrophoresis; Female; Globulins; Glycoproteins; Haptoglobins; Heart Failure; Humans; Hydrogen-Ion Concentration; Immunoglobulin A; Immunoglobulin G; Lung Diseases; Macroglobulins; Male; Middle Aged; Muramidase; Sputum; Transferrin; Trypsin Inhibitors; Ultracentrifugation