Shock and Tissue Injury Induced by Recombinant Human Cachectin

DOI Web Site 被引用文献62件
  • Kevin J. Tracey
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • Bruce Beutler
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • Stephen F. Lowry
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • James Merryweather
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • Stephen Wolpe
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • Ian W. Milsark
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • Robert J. Hariri
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • Thomas J. Fahey
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • Alejandro Zentella
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • James D. Albert
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • G. Tom Shires
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
  • Anthony Cerami
    Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.

抄録

<jats:p>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.</jats:p>

収録刊行物

  • Science

    Science 234 (4775), 470-474, 1986-10-24

    American Association for the Advancement of Science (AAAS)

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