伏核在躯体传入冲动抑制防御性心血管反应中的作用及机制

损毁伏核可明显削弱电刺激腓深神经（ＤＰＮ）对兴奋下丘脑背内侧核诱发的升压反应和心肌缺血的抑制作用（Ｐ＜０．０５，Ｐ＜０．０１）。电刺激伏核可引起明显的降压效应。中脑中央灰质腹侧部（ｖＰＡＧ）微量注射纳洛酮可明显衰减伏核的减压效应；损毁ｖＰＡＧ甚至可翻转伏核的减压效应，引起轻度升压（Ｐ＜０．０１）。损毁弓状核后伏核的减压效应基本消失，弓状核内微量注射纳洛酮明显衰减伏的的减压效应。故ＤＰＮ传入冲动可能

THE ROLE OF ACCUMBENS NUCLEUS IN THE INHIBITORY EFFECT OF SOMATIC AFFERENT INPUTS ON THE DEFENCE CARDIOVASCULAR RESPONSE AND ITS MECHANISM

After Accumbens Nucleus (AC) lesion, the inhibitory effect of deep Peroneal nerve (DPN) on the pressor response and ECG-ST changes induced by excitation of dorsomedial nucleus of hypothalamus (DMH) was decreased as compared with that of before lesion (P<0. 05, P<0. 01). Electrical stimulation of AC could elicit prominent depressor response, which could be effectively lessened by microinjection of naloxone into ventral periaqueductul gray (vPAG). Lesion of vPAG could reverse the depressor response to AC stimulation to a slight pressor response (P<0. 01 ). After lesion of arcuate nucleus of hypothalamus (ARC), the depressor response to AC stimulation almost disappeared, which, again, could be largely mimicked by microinjection of naloxone into ARC.