Amir S, Harel M
Arch Toxicol Suppl. 1983;6:261-5. doi: 10.1007/978-3-642-69083-9_48.
This study assessed the role of endogenous opiate systems in the hyperglycemic response to endotoxin challenge in mice. Blockade of opiate receptors by administration of the opiate antagonists naloxone (1.0 mg/kg) or naltrexone (1.0 or 5.0 mg/kg) significantly lessened to degree of hyperglycemia cause by endotoxin challenge (80 micrograms). Methyl naltrexone, a peripherally acting opiate antagonist, had no demonstrable effect on endotoxin-induced hyperglycemia. Finally, induction of tolerance to morphine prevented the hyperglycemic response to endotoxin challenge. These results suggest a causative role for central nervous system endorphinergic mechanisms in the hyperglycemic response to endotoxin administration. They support the view that centrally acting opiate antagonist, by blocking the brain opiate receptors, can influence metabolic adaptation to endotoxin shock.
本研究评估了内源性阿片系统在小鼠对内毒素刺激的高血糖反应中的作用。通过给予阿片拮抗剂纳洛酮（1.0毫克/千克）或纳曲酮（1.0或5.0毫克/千克）来阻断阿片受体，可显著减轻内毒素刺激（80微克）所引起的高血糖程度。甲基纳曲酮是一种外周作用的阿片拮抗剂，对内毒素诱导的高血糖没有明显影响。最后，诱导对吗啡的耐受性可防止对内毒素刺激的高血糖反应。这些结果表明，中枢神经系统内啡肽能机制在对内毒素给药的高血糖反应中起因果作用。它们支持这样一种观点，即中枢作用的阿片拮抗剂通过阻断脑内阿片受体，可影响对内毒素休克的代谢适应。
