Changes in the Motor Evoked Potentials Produced by Stimulation of Reticulospinal Tract Neurons in the Chronic Spinal Cord Injury of Rat / 대한척추외과학회지

STUDY DESIGN: There is a prospective study of 80 Sprague-Dawley rats which were made at the spinal cord lesion T5/6 level, sparing only one ventral quadrant. We monitered medullary reticulospinal neurons(RtN) evoked potentials at the L2/3 level which laminectomy was performed. OBJECTIVE: to investigate changes in the physiological responses of motor neurons to stimulation of the medullary reticular formation following partial spinal cord lesions sparing only the ventral quadrant. SUMMERY AND BACK GROUND DATA: There were many report that the animals with spinal cord lesion recovered well-coordi-nated fourlimb locomotion within 2-3 weeks. The time course of the functional recovery of this hindlimb locomotion was cor-related with the recovery of motor evoked potentials(MEP), which originate from reticular nuclei. Therefore, it was hypothe-sized that the return of locomotor function after incomplete spinal cord injury may partially rely on the reorganization of descending inputs to ventral horn neurons previously occupied by damaged afferents. MATERIALS AND METHODS: Total 80 Sprague-Dawley rats were used in this study. Under sterile conditions, spinal cord lesions were made at the T5/6 level using a No. 11 blade, sparing only one ventral quadrant. The animals allowed to survive from one day to 61 days. To monitor RtN evoked potentials, laminectomies were performed at L2/3 level. Field potentials were recorded using a glass microelectrode filled with 2 M NaCl(1.5-2.0 M Ohm). Cord dorsum potentials were also epidurally monitored at L2/3 using a pair of teflon-coated wires. The gigantocellular reticular nucleus ipsilateral to the spared ventral cord was stimulated using a monopolar tungsten microelectrode. RESULTS: The field potentials generated in the ventral horn of the lumbar cord were recorded bilaterally. In some animals field potentials were monitored just before and right after the spinal cord lesion. 1) Following spinal cord lesion at T5/6, the amplitude of RtN evoked potentials declined significantly in the L2/3 ventral gray matter of the completely lesioned side. Field potentials monitored below the ipsilaterally spared ventral quadrant remained unchanged. Depressed RtN evoked potentials in the ventral cord gradually increased during the next four weeks, and finally reached greater than 4 times of the amplitude monitored on the contralateral side. 2) The sites in which field potentials could be monitored in the lumbar spinal cord were mapped. In normal rats, the largest field was monitored near the ventral margin of the gray matter. On the other hand, in spinal cord injured ani-mals, the largest field potentials were located in more dorsal aspects of the ventral horn, suggesting a structural reorganization of the descending inputs has taken place. CONCLUSION: The RtN evoked potentials in the ventral horn increased gradually for several weeks after the injury. The returned RtN evoked potentials below the completely lesioned side of spinal cord were larger than those seen in normal spinal cord. The time course of returning evoked potentials below the lesioned side of the spinal cord seems to coincide with the resti-tution of same-side hindlimb locomotion.

Effect of Diltiazem and Verapamil on Pipecuronium-and Atracurium-induced Neuromuscular Blockade / 대한마취과학회지

The effects and interactions of pipecuronium and atracurium with diltiazem and verapalmil on the electrically-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat phrenic-hemidiaphragm preparation. Pipecuronium (3X10(-7) -4X10(-6)) and atracurium (10(-6) -3X10(-5) M) decreased the electrically-evoked twitch response, train-of-four and tetanus ratio in a dose-related fashion and the pipecuronium was more potent than atracurium. The inhibitory effects of pipecuronium and atracurium were potentiated by pretreatment of 5 uM diltiazem and verapamil, Ca++-channel blokers, in which the concentration of diltiazem or verapamil has no obvious effect on the twitch response itself. Futhermore, it is noteworthy that the inhibitory effects of pipecuronium and atraeurium were markedly potentiated by 150 uM hemicholinium pretreatment. On the basis of these findings, the results of present study suggests that the muscle relaxation by pipecuronium and atracurium is mediated by pre- and post-junctional receptor blockade, and that diltiazem or verapamil intensifies neuromuscular blockade produced by these musele relaxants. The potentiating effect of diltiazem or verapamil may be due to blocking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.

Effect of Diltiazem on Pancuronium - and Vecuronium - induced Neuromuscular Blockade / 대한마취과학회지

The effects and interactions of pancuronium and vecuronium with diltiazem on the electri- cally-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat hemi-diaphragm preparation. Pancuronium(3 X 10(-7) -10(-5) M) and vecuronium(3 X 10(-6)-15 X 10(-6) M) decreased the electrically evoked(nerve stimulation, 0.1Hz, 0.5ms, 10V) twitch response, train-of-four and tetanus ratio in a dose-related fashion and pancuronium was more potent than vecuronium. The inhibitory effects of pancuronium and vecuronium were potentiated by pretreatment with 5 & 10 uM diltiazem, a Ca++-channel blocker, in which the concentration of diltiazem has no obvious effects on the twitch response itself. Furthermore, it is noteworth that the inhibitory effects of pancuronium and vecuronium were markedly potentiated by 150 uM hemicholinium pretreatment. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, pancuronium and vecuronium decreased the electrically evoked twitch response dose dependently, but the amplitudes of inhibition were less than those in indirect(nerve) stimulation. The inhibitory effects were not affected by diltiazem pretreatment except low doses of vecuronium. On the basis of these findings, the result of the present study suggests that the muscle relaxation by pancuronium and vecuronium is mediated by pre- and post-junctional receptor blockade, and that diltiazem intensifies neuromuscular blockade produced by muscle relaxants. The potentiating effect of diltiazem may be due to blocking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.

Effect of Diltiazem on Pancuronium - and Vecuronium - induced Neuromuscular Blockade / 대한마취과학회지

The effects and interactions of pancuronium and vecuronium with diltiazem on the electri- cally-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat hemi-diaphragm preparation. Pancuronium(3 X 10(-7) -10(-5) M) and vecuronium(3 X 10(-6)-15 X 10(-6) M) decreased the electrically evoked(nerve stimulation, 0.1Hz, 0.5ms, 10V) twitch response, train-of-four and tetanus ratio in a dose-related fashion and pancuronium was more potent than vecuronium. The inhibitory effects of pancuronium and vecuronium were potentiated by pretreatment with 5 & 10 uM diltiazem, a Ca++-channel blocker, in which the concentration of diltiazem has no obvious effects on the twitch response itself. Furthermore, it is noteworth that the inhibitory effects of pancuronium and vecuronium were markedly potentiated by 150 uM hemicholinium pretreatment. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, pancuronium and vecuronium decreased the electrically evoked twitch response dose dependently, but the amplitudes of inhibition were less than those in indirect(nerve) stimulation. The inhibitory effects were not affected by diltiazem pretreatment except low doses of vecuronium. On the basis of these findings, the result of the present study suggests that the muscle relaxation by pancuronium and vecuronium is mediated by pre- and post-junctional receptor blockade, and that diltiazem intensifies neuromuscular blockade produced by muscle relaxants. The potentiating effect of diltiazem may be due to blocking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.