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  • 1
    Publikationsdatum: 1986-03-07
    Beschreibung: A sensitive radioimmunoassay for atrial natriuretic peptide was used to examine the relation between circulating atrial natriuretic peptide and cardiac filling pressure in normal human subjects, in patients with cardiovascular disease and normal cardiac filling pressure, and in patients with cardiovascular disease and elevated cardiac filling pressure with and without congestive heart failure. The present studies establish a normal range for atrial natriuretic peptide in normal human subjects. These studies also establish that elevated cardiac filling pressure is associated with increased circulating concentrations of atrial natriuretic peptide and that congestive heart failure is not characterized by a deficiency in atrial natriuretic peptide, but with its elevation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnett, J C Jr -- Kao, P C -- Hu, D C -- Heser, D W -- Heublein, D -- Granger, J P -- Opgenorth, T J -- Reeder, G S -- New York, N.Y. -- Science. 1986 Mar 7;231(4742):1145-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2935937" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Aged ; Atrial Natriuretic Factor/*blood ; Cardiovascular Diseases/blood ; Female ; Heart Failure/*blood ; Hemodynamics ; Humans ; Male ; Middle Aged ; Radioimmunoassay
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 1986-10-24
    Beschreibung: Cachectin (tumor necrosis factor), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin. Recombinant human cachectin was infused into rats in an effort to determine whether cachectin, by itself, can elicit the derangements of host physiology caused by administration of endotoxin. When administered in quantities similar to those produced endogenously in response to endotoxin, cachectin causes hypotension, metabolic acidosis, hemoconcentration, and death within minutes to hours, as a result of respiratory arrest. Hyperglycemia and hyperkalemia were also observed after infusion. At necropsy, diffuse pulmonary inflammation and hemorrhage were apparent on gross and histopathologic examination, along with ischemic and hemorrhagic lesions of the gastrointestinal tract, and acute renal tubular necrosis. Thus, it appears that a single protein mediator (cachectin) is capable of inducing many of the deleterious effects of endotoxin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tracey, K J -- Beutler, B -- Lowry, S F -- Merryweather, J -- Wolpe, S -- Milsark, I W -- Hariri, R J -- Fahey, T J 3rd -- Zentella, A -- Albert, J D -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):470-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3764421" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blood Glucose/metabolism ; Endotoxins/toxicity ; Female ; Glycoproteins/*toxicity ; Humans ; Potassium/blood ; Rats ; Recombinant Proteins ; Shock/*chemically induced/pathology/physiopathology ; Sodium/blood ; Tumor Necrosis Factor-alpha
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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