Bhattacharya S K, Das N
Neurochem Pathol. 1984 Fall;2(3):163-9. doi: 10.1007/BF02834350.
Carrageenin-induced pedal inflammation in rats, was found to significantly enhance brain levels of prostaglandin (PG) E2 and PGF2 alpha. PG levels increased after 30 min of induction of the inflammation, peaked at 1 h, and attained normal levels by 4 h. Bilateral adrenalectomy had little effect on carrageenin-induced increase in rat brain PGs. The pattern of elevation of central PGs and the time course of carrageenin inflammation were at variance, the latter peaking between 3 and 4 h. The findings lend credence to the postulate that inflammatory hyperalgesia involves participation of central pain circuits, and that fever accompanying inflammation is caused by the central release of PGs. The central nociceptive and hyperthermic actions of PGs are well documented. However, the increase in central PG levels may well be caused by stress induced by the peripheral inflammation, since the pattern of elevation in either case is qualitatively similar.
在大鼠中发现，角叉菜胶诱导的足爪炎症可显著提高大脑中前列腺素（PG）E2和PGF2α的水平。炎症诱导30分钟后PG水平升高，1小时达到峰值，4小时恢复正常水平。双侧肾上腺切除术对角叉菜胶诱导的大鼠脑PG增加影响不大。中枢PG升高的模式与角叉菜胶炎症的时间进程不一致，后者在3至4小时达到峰值。这些发现支持了以下假设：炎症性痛觉过敏涉及中枢疼痛回路的参与，并且炎症伴随的发热是由PG的中枢释放引起的。PG的中枢伤害感受和体温升高作用已有充分记录。然而，中枢PG水平的升高很可能是由外周炎症诱导的应激引起的，因为在这两种情况下升高的模式在质量上是相似的。
