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Shock and tissue injury induced by recombinant human cachectin
Science (New York, N.Y.)
|October 24, 1986
Summary
Cachectin, also known as tumor necrosis factor, causes severe physiological damage and death in rats. This protein alone can induce hypotension, acidosis, and organ damage, mimicking endotoxin effects.
Area of Science:
- Biochemistry
- Immunology
- Pathophysiology
Background:
- Cachectin (tumor necrosis factor) is a protein produced by macrophages activated by endotoxin.
- Cachectin is believed to mediate the lethal effects of endotoxin.
Purpose of the Study:
- To investigate if cachectin alone can induce the physiological derangements caused by endotoxin administration.
- To determine the direct effects of cachectin on host physiology.
Main Methods:
- Recombinant human cachectin was infused into rats.
- Physiological parameters, blood chemistry, and post-mortem examinations were analyzed.
Main Results:
- Cachectin infusion caused hypotension, metabolic acidosis, hyperglycemia, and hyperkalemia.
- Rats exhibited hemoconcentration, respiratory arrest, and death within hours.
- Necropsy revealed pulmonary inflammation, gastrointestinal lesions, and renal tubular necrosis.
Conclusions:
- Cachectin, as a single protein mediator, can induce many deleterious effects previously attributed to endotoxin.
- This study highlights cachectin's significant role in endotoxin-induced toxicity.