Abstract
Summary
The administration of Salmonella enteritidis endotoxin to male rats rendered hypersensitive by lead acetate resulted in profound hypoglycemia, lactacidemia, and depletion of liver glycogen. Lead acetate depressed gluconeogenesis as studied in isolated hepatocytes. Possible mechanisms for lead's action on gluconeogenesis and the significance of this metabolic lesion in lead hypersensitivity to shock are discussed.
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