Abstract
To delineate possible mechanisms of lead acetate enhancement to endotoxin shock, liver parenchymal, and Kupffer cell function were evaluated in lead acetate-treated rats receiving low doses of S. enteritidis endotoxin. Additionally, the influence of methylprednisolone and cysteine, agents which have been demonstrated to prevent lead-induced endotoxin lethality was ascertained. Rats receiving lead acetate demonstrated profound hyperreactivity to endotoxin as denoted by increased mortality, impairment of bromsulphalein (BSP) removal, hypoglycemia, and increased blood lactate and pyruvate. Plasma activity of glutamic pyruvic transaminase (GPT), glutamic oxalacetic transaminase (GOT), and alkaline phosphatase was strikingly elevated. Serum activity of beta-glucuronidase and plasma acid phosphatase was also elevated. Methylprednisolone or cysteine treated rats were essentially refractory to the lethal effects of lead acetate and endotoxin. The enhanced survival of lead-endotoxin treated rats following administration of methylprednisolone or cysteine was associated with reduced impairment in BSP removal, a normal blood glucose, and significant reductions in blood lactate and pyruvate. Plasma activity of GPT, GOT, and alkaline phosphatase was also reduced. Slight reductions were observed in plasma activity of acid phosphatase although serum beta-glucuronidase activity was not significantly altered. Phagocytic activity, as measured by hepatic uptake of gelatinized RE test lipid emulsion, indicated a hypofunctional state of Kupffer cells in lead acetate-endotoxin treated rats. Since neither methylprednisolone, nor cysteine treatment modified the hypophagocytic state, Kupffer cell phagocytic dysfunction does not appear to play a major role in enhanced endotoxin susceptibility of lead acetate treated rats. The maintenance of parenchymal cell function in methylprednisolone or cysteine treated rats injected with lead and endotoxin supports the hypothesis of a contributory role for hepatic parenchymal cells in the pathophysiology of lead-endotoxin interaction.
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