摘要
实验观察了前列腺素 (prostaglandins ,PGs)合成限速酶 非选择性环氧合酶 (cyclo oxygenase,COX)抑制剂消炎痛和外源性前列腺素E2 (prostaglandinE2 ,PGE2 )对糖尿病痛过敏大鼠隐神经中Aδ 单位和C单位传入活动的影响。结果发现 ,糖尿病痛过敏大鼠Aδ 单位和C单位的传导速度和它们的机械阈值显著降低 ,少数Aδ 单位 (4/ 2 4 )和C单位 (2 / 18)具有自发活动。腹腔注射消炎痛后能明显缓解糖尿病痛过敏大鼠的机械性痛过敏 ,并抑制自发放电。在消炎痛阻断内源性PGs合成后 ,外源性PGE2 能使糖尿病痛过敏组和对照组大鼠Aδ 单位和C单位的机械阈值显著降低 ,并诱发糖尿病痛过敏组大鼠 3个Aδ 单位 (3/ 2 4 )和 1个C单位 (1/ 18) ,以及对照组大鼠 2个Aδ 单位 (2 / 13)产生传入活动。结果提示 ,在患糖尿病性神经病时 ,PG的合成和释放增多 ,这些PGs敏化或和激活Aδ 单位和C单位 。
The effects of a non selective inhibitor of cyclo oxygenase (COX) indomethacin, and exogenous prostaglandin E 2 (PGE 2) on A δ units and C units in the saphenous nerve of diabetic hyperagesic rats were studied The results showed that the conduction velocity of A δ units and C units and their mechanical threshold in diabetic hyperagesic rats were obviously decreased, and a small number of A δ units (4/24) and C units (2/18) produced increased spontaneous activities Intraperitoneal injection of indomethacin in diabetic hyperagesic rats significantly relieved mechanical hyperalgesia, and resulted in a decrease in spontaneous afferent activities of the A δ units and C units Subcutaneous injection of exogenous PGE 2 into the diabetic hyperagesic and control rats produced a significant decrease in mechanical threshold of the A δ units and C units, and elicited discharge from 3 A δ units (3/24) and 1 C unit (1/18) in diabetic hyperagesic rats and from 2 A δ units (2/13) in control rats The present data suggest that the synthesis and release of PGs are increased in diabetic neuropathy, PGs can sensitize and /or activate A δ units and C units and elicit hyperagesia and allodynia in diabetic rats
出处
《生理学报》
CAS
CSCD
北大核心
2002年第5期379-394,共16页
Acta Physiologica Sinica
