延髓头端腹内侧区对大鼠心脏伤害性感受的下行调控作用

目的观察延髓头端腹内侧区（rostroventral medulla, RVM）对大鼠心脏伤害性感受的下行调控作用。方法通过心包插管
术制作心脏-躯体运动反射（cardiosomatic motor reflex, CMR）大鼠模型，采用RVM电刺激（强度分别为25、75 和100 μA）及
RVM电损毁的方法，以心包内可复性注入致痛剂辣椒素（capsaicin, CAP）所诱发的背斜方肌肌电（EMG）为指标评估RVM对心
脏伤害性感受的下行调控作用。结果RVM内8个刺激位点对CAP注射诱发的EMG反应产生了强度依赖性的抑制作用（F[2,
21]=43.188，P=0.001）；3个刺激位点产生了完全易化效应，其易化的程度与刺激强度无关（F[2,6]=0.884，P=0.461）；11个刺激位点对
CAP注射诱发的EMG反应产生了双向调节作用，即低强度（25 μA）刺激，EMG反应明显大于基础对照（P<0.05），高强度（75/
100 μA）刺激，EMG反应明显低于基础对照（P<0.05）；RVM实施电损毁后，EMG反应明显高于损毁前及假损毁组（P<0.05）。结
论心脏受到伤害性刺激后，RVM对大鼠心脏伤害性感受具有双向调控作用，且以下行抑制性调控作用为主。

Descending modulation of cardiac nociception by the rostral ventromedial medulla in rats

Objective To observe the descending modulation of cardiac nociception by the rostral ventromedial medulla (RVM)
in rats. Methods A rat model of cardiosomatic motor reflex (CMR) was established by injecting capsaicin into the pericardial
sac to induce cardiac nociception, and the electromyogram (EMG) response of the dorsal spinotrapezius muscle was studied.
The RVM was electricaly stimulated (25, 75 and 100 μA) or destroyed to examine whether RVM exerted descending
modulation on cardiac nociception. Results Electrical stimulation of the RVM at 8 sites produced intensity-dependent
inhibition of EMG responses to noxious cardiac stimulus (F[2,21] =43.188, P=0.001). Electrical stimulation at 3 sites caused
facilitated EMG responses, but the increased magnitude of the EMG was not dependent on stimulation intensity (F[2,6]=0.884, P=
0.461). Stimulation at 11 sites produced biphasic effects: at a low intensity (25 μA), the elicited EMG magnitude was
significantly larger than baseline (P<0.05), and at greater intensities (75/100 μA), the stimulation caused suppression of the
EMG magnitude to a level significantly lower than the baseline (P<0.05). Electrolytic lesion of the RVM resulted in significantly
increased EMG responses compared with the baseline and sham lesion group. Conclusion Cardiac nociception evoked by
capsaicin stimulation is subjected to descending biphasic modulation by the RVM, which produces predominantly descending
inhibition on heart pain.