大鼠顶盖前区前核内去甲肾上腺素α_2受体对心脏-躯体运动反射的调制

Norepinephrine α_2 receptor in the anterior pretectal nucleus of rats participates in the modulation of the cardiosomatic motor reflex

目的:观察顶盖前区前核(the anterior pretectal nucleus,APtN)内的去甲肾上腺素α_2受体是否参与大鼠急性心脏痛导致的心脏-躯体运动反射(cardiosomatic motor reflex,CMR)的调制。方法:SD雄性大鼠麻醉后行心包插管术,经管给予辣椒素(1μg/ml,0.2 ml)诱导急性炎性心脏痛模型。颅内插管,经管向APtN内微量注射药物。将同芯电极插入对侧背斜方肌内,记录心脏痛和APtN药物注射(0.2μl)对其肌动电流图(electromyogram,EMG)的影响。结果:(1)APtN内分别微量注射非选择性去肾上腺素受体激动剂去甲肾上腺素2μg或4μg,可明显抑制心包内注射辣椒素诱发的背斜方肌肌电。EMG反应相对于基础对照分别减小至37.6%±3.75%及16.9%±3.57%;(2)APtN内微量注射选择性α_2受体激动剂可乐定2μg或4μg,心包内辣椒素诱发的背斜方肌EMG相对于基础对照分别减小至54.3%±4.15%和36.2%±4.01%。(3)APt N内预先注射α_2受体拮抗剂育亨宾则可减弱可乐定的抑制作用,心包内注射辣椒素诱发的EMG增至89.2%±4.01%。结论:APtN内的去甲肾上腺素对于大鼠CMR存在明显抑制效应,该效应可能主要由α_2受体介导。

Objective： To examined the role of the anterior pretectal nucleus（ APtN） and norepinephrine（ NE） α2 receptors in the modulation of cardiosomatic motor reflex（ CMR） induced by acute cardiac pain in rats. Methods： SD male rats were anesthetized and a silicone rubber catheter was inserted into the pericardial sac. Capsaicin injection（ 1 μg/ml,0. 2 ml） was applied pericardially through the catheter to induce acute inflammatory cardiac pain. A 1 μl microsyringe was inserted into the APtN and 0. 2 μl of drugs were infused. A concentric electrode was inserted into the left spinotrapezius muscle to record the electromyogram（ EMG） activity. The effect of capsaicin-induced acute cardiac pain and APtN drugs application on the EMG response were observed. Results：（ 1） Microinjection of NE（ 2 or 4 μg）into APtN significantly inhibited the CMR. The EMG responses decreased to 37. 6% ± 3. 75% or 16. 9% ± 3. 57% of the baseline,respectively.（ 2） Microinjection of NE α2 receptor agonist clonidine into the APtN（ 2 or 4 μg） decreased the EMG responses to 54. 3% ± 4. 15% or 36. 2% ± 4. 01% of the baseline.（ 3） Pretreatment with α2 receptor antagonist yohimbine at the same APtN site antagonized the effect of following clonidine injection and the EMG responsesincreased to 89. 2% ± 4. 01% of the baseline. Conclusion： These findings suggest that NE in APtN is involved in the inhibition of CMR,which is largely mediated by the α2 receptor.