目的 :阐明杏仁及中枢阿片肽类递质在躯体传入冲动对下丘脑室旁核 (PVN)兴奋诱发的心血管活动的调节效应中的作用。方法 :采用电刺激及多管玻璃微电极脑内微量注射法

观察在侧脑室或同侧杏仁中央核 (ACe)微量注射阿片受体阻断剂纳洛酮后

躯体传入冲动对兴奋PVN诱发的心血管反应的影响。结果 :电刺激一侧PVN后

平均动脉压 (MAP)升高。电刺激腓深神经(DPN)对上述反应有部分抑制作用 (P <0 .0 1 )

DPN对升压的抑制百分比为 43 .2 9%。电刺激DPN也能抑制一侧PVN微量注射L 谷氨酸钠 (L SodiumGlutamate

Glu) 1 0 0nL引起的升压效应

抑制百分比为 64.58%。侧脑室注射纳洛酮 ( 3 0 μg/ 1 5μL)可部分阻断DPN的上述抑制作用

DPN对升压的抑制百分比由 56.67%下降到 1 3 .79%

抑制取消了 42 .88%。杏仁注射纳洛酮( 2 0 0ng/ 1 0 0nL) 也削弱刺激DPN对刺激PVN诱发的升压反应的抑制作用

DPN对升压的抑制百分比由 60 .1 9%下降到 2 1 .0 5% (P <0 .0 1 )

抑制削弱了 3 9.1 4 %。结论 :杏仁及中枢阿片肽参与DPN传入冲动对PVN中枢性心血管反应的抑制作用Objective: To analyze the role of amygdala and central opioid peptide in somatic afferent input induced suppression of the cardiovascular response to electrical stimulation of the paraventricular nucleus of the hypothalamus (PVN). Methods:SD rats anesthetized using 20% urethane (1.0～ 1.2 g/kg) were used in this study. In accordance with Paxinos and Watson's Rat Brain Stereotaxic Atlas

a bipolar stainless stimulating electrode was inserted into PVN for giving central electrical stimulation. Multibarreled micropipettes (about 50 μm in tip diameter) were employed for microinjection of L sodium glutamate

naloxone or normal saline into the lateral ventricule or amygdala. Deep peroneal nerve (DPN) was stimulated with electric current 0.3 ～0.4 mA

frequency of 4 Hz

0.5 ms of duration of wave wideth and 5 min of stimulation duration. The stimulating parameters of PVN were 0.1～ 0.3 mA

80 Hz

0.5 ms (wave wideth) and 10 sec (duration of stimulation). Results: Electrical stimulation of PVN caused increase of mean arterial pressure (MAP). Electrical stimulation of DPN could significantly inhibit PVN stimulation induced increase of MAP(P<0.01)

with the inhibitory percentage of pressor response being 43.29%. Stimulation of DPN could also inhibit the pressor response induced by introducing L sodium glutamate (100 nL in 0.5 M) into PVN. The inhibitory percentage of pressor response was 67.11%. Administration of naloxone (30 μg/15 μL) into lateral ventricle of brain reduced the inhibitory effect of DPN stimulation. The inhibitory percentage decreased from 56.67% to 13.79%. Administration of naloxone (0.2 μg/0.1 μL) into amygdalaalso reduced the inhibitory effect of DPN stimulation. The inhibitory percentage decreased from 60.19% to 21.05% (P<0.01). Conclusion: Central opioid receptor and amygdala are involved in the inhibitory effect of DPN stimulation on central pressor response.