躯体传入冲动抑制中枢性心肌缺血的脊髓机制

本工作在58只尿酯-氯醛糖麻醉,三碘季铵酚制动,人工呼吸,切断迷走神经的兔上进行。结果显示:电刺激正中神经(MN)和腓深神经(DPN)均能抑制或部分抑制下丘脑背内侧核(DMH)诱发的缺血性心电 ST 段偏移,以刺激 MN 的抑制作用更为明显。蛛网膜下腔注射(ith)吗啡(40μg)也能抑制这种缺血性心电变化。ith 纳洛酮(20μg)则可阻断刺激 MN 对中枢性心肌缺血的抑制作用。完整兔在刺激左侧 MN 或 DPN 后,用放射免疫技术测得胸 2—5(T_2-5)节段两侧中间外侧柱(IML)中亮氨酸脑啡肽(LENK)含量明显增加。在颈1(C_1)水平横断脊髓,以同样参数刺激左侧 MN,同侧胸髓 IML 中 LENK 含量明显增加,而对侧胸髓 IML 中 LENK 含量无明显改变;刺激一侧 DPN,T_(2-5)的两侧 IML 中 LENK 含量均无明显变化。上述结果表明,刺激 MN 与 DPN 均能抑制 DMH 诱发的中枢性心肌缺血,但以MN 作用较明显。我们推测这种抑制作用可能与通过脊上机制双侧性增加 IML 中 LENK 含量有关,MN 的抑制作用可能尚包括直接激活胸髓内的脑啡肽系统,增加同侧 IML 中 LENK含量,加强了对交感输出活动的抑制作用。

SPINAL MECHANISM OF THE INHIBITORY EFFECT OF SOMATIC INPUT ON THE CARDIAC ISCHEMIA INDUCED BY HYPOTHALAMUS STIMULATION

Experiments were carried out on 58 urethane-chloralose anaesthetized, gallamine triethiodide immobilized and vagotomized rabbits under artificial ventilation. Median nerve (MN) or deep peroneal nerve(DPN) stimulation could inhibit completely or partially the deflection of ischemic ECG ST segment due to stimulation of dorsomedial hypothalamic nucleus (DMH). The inhibitory effect of MN stimulation was more marked than that of DPN stimulation. Intrathecal injection (ith) of morphine (40 micrograms) could also inhibit these ischemic ECG ST segment changes. After ith naloxone (20 micrograms), the inhibitory effect of MN stimulation on DMH stimulation-induced ischemic ECG ST segment changes was abolished. In intact rabbits, it was demonstrated that L-enkephalin (LENK) immunoreactive material was increased in the left or right intermediolateral cell column (IML) of T2-5 spinal cord after stimulation of left MN or DPN for five minutes. In the Cl transected rabbits, stimulation of MN only increased ipsilateral LENK immunoreactive material content in the thoracic IML, while stimulation of DPN produced no such an effect. These results indicate that stimulation of MN or DPN can inhibit cardiac ischemia induced by DMH stimulation and that the effect of MN stimulation is more potent. The inhibitory effects may be mediated by an increase of LENK immunoreactive material in the bilateral IML produced through some supraspinal mechanisms; whereas the effect of MN stimulation may also be mediated by an increase of ipsilateral spinal LENK immunoreactive material in the thoracic IML through segmental mechanism to inhibit the sympathetic activity.