[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.