交感传出在大鼠糖尿病性痛过敏中的作用

交感传出和前列腺素（ＰＧｓ）在周围神经不全损伤和炎症所引起的痛过敏中起重要作用，它们对糖尿病性痛过敏影响尚不清楚。本工作先给大鼠腹腔注射６－羟多巴胺（６－ＯＨＤＡ）损毁交感节后神经元（ＳＰＧＮｓ）末梢后，再给予链脲佐菌素（ＳＴＺ）以建立６－ＯＨＤＡ糖尿病大鼠模型，在连续４周的观察中这组大鼠伤害性爪回缩阈值（ＮＰＷＴ）和甩尾反向潜伏期（ＴＥＬ）没有明显变化，而糖尿 病组大鼠的痛阈显著降低，并伴有痛过

EFFECTS OF SYMPATHETIC EFFERENT IN DIABETIC HYPERALGESIA IN RAT

While sympathetic efferents and prostaglandins (PGs) play an important role inhyperalgesia of partial injury of peripheral nerves and inflammation, whether these arealso involved in diabetic hyperalgesia is unknown. With intraperitoneal injection of 6-hydroxydopamine (6-OHDA) to eliminate effects of sympathetic postganglionic neurons (SPGNs) terminals, a model of diabetic rats with infused 6-OHDA could be set upby injection of streptozotocin (STZ). Nociceptive paw-withdrawal threshold (NPWT)and tail flick latency (TFL) in 6-OHDA/diabetic rats were not changed significantly inthe following four weeks. However, in diabetic group rats, pain threshold was decreased significantly and accompanied by development of hyperalgesia. NPWT was significantly decreased with noradrenaline (NA) in diabetic hyperalgesic rats and increased with phentolamine or yohimbine, but not by prazocin. In the control rats,NPWT are not changed significantly by NA or phentolamine, and in 6-OHDA/diabeticrats, neither NA nor phentolamine also affected on NPWT significantly. However,NPWT may be significantly decreased by PGEI, PGE2 and PGD2 in both the controland the diabetic hyperalgesic rats. The above results suggested that SPGNs terminals areinvolved in hyperalgesia of diabetic rats, NA accelerated synthesis of PGs and releasedby way of presynaptic effect on a2-adrenergic receptors at the SPGNs terminals, PGs,in turn, directly acted on the primary afferent nociceptors, producing hyperalgesia.