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Endotoxin protection against pulmonary oxygen toxicity and plasma prostaglandin levels in the rat.

作者信息

Klein J, Trouwborst A, Erdmann W

机构信息

Department of Anaesthesia, Erasmus University Rotterdam, The Netherlands.

出版信息

Adv Exp Med Biol. 1987;215:355-8. doi: 10.1007/978-1-4684-7433-6_42.

DOI:10.1007/978-1-4684-7433-6_42
PMID:3478992
Abstract

Exposure of rats to high concentrations of oxygen (greater than 95%) at 1 ATA pressure (101 kPa) is lethal within three days. Rats treated with a small dose of endotoxin are protected against these lethal effects of hyperoxia. Recently, we found that the lysine salt of acetylsalicylic acid antagonises this protective action of endotoxin. This suggests that prostaglandin metabolism plays an important role in the protective action of endotoxin against pulmonary oxygen toxicity. Therefore, we measured the plasma levels of 6KPGF1 alpha, a stable degradation product of prostacyclin (PGI2), PGE2 and thromboxane B2, the stable degradation product of thromboxane A2, in rats exposed to air or greater than 95% oxygen for 48 hours. We compared these with the plasma levels of rats treated with endotoxin (Salmonella typhimurium lipopolysaccharide 1 mg/kg) and exposed to air or greater than 95% oxygen for 48 hours. We found that exposure of rats to greater than 95% oxygen for 48 hours leads to a significant rise in the 6KPGF1 alpha levels. Rats exposed to greater than 95% oxygen for 48 hours and treated with endotoxin had significantly higher PGE2 and significantly lower 6KPGF1 alpha plasma levels than saline-treated rats exposed to greater than 95% oxygen for 48 hours.

摘要

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