Evaluation for action mechanism of Alpha2-agonist dexmedetomidine to respiratory center in medulla

我给药右美托咪定，这是本研究的实验组，并与大鼠脑干脊髓制备，研究呼吸中枢的活动。将标本上升至灌流罐中，用95%O_2、5%CO_2饱和，在人工脑脊液中灌流。作为呼吸神经元活动输出的监测器，它是通过C4前根用吸收电极记录吸气活动。将右美托咪定灌流于灌流液中，连续记录呼吸抑制时呼吸输出的活动特征和呼吸变化发生相关神经元的活动特征。结果显示，右美托咪定呈剂量依赖性抑制呼吸神经元活性。然而，在呼吸神经元的活动特性中，通过一般临床使用密度没有认识到明显的影响。至于高密度相关神经元活动中呼吸的抑制，提示通过刺激α-肾上腺素受体的间接影响，并且似乎右美托咪定对延髓中的呼吸神经元几乎没有直接影响。

I administer dexmedetomidine which is the experimental group of this study and, with a rat brainstem spinal cord preparation, investigate the activity of the respiratory center. It is perfusion in the artificial cerebrospinal fluid which the specimen rises to perfusion tank, and was saturated with 95%O_2, 5% CO_2. As a breathing of the respiratory neuron activity output monitor, it is recorded inspiratory activity with an absorption electrode by a C4 ventral root. I administer dexmedetomidine in perfusion liquid and record the activity characteristics output of the breathing when respiratory depression and a breathing change occur-related neuron continually. As for the result, respiratory neuron activity was depressed dose-dependency by dexmedetomidine. However, the clear influence was not recognized in activity characteristics of the respiratory neuron by the general clinical use density. As for the restraint of the breathing in the high density-related neuron activity, indirect influence by the stimulation of the alpha-adrenoreceptor was suggested, and it seemed that there was little direct influence of dexmedetomidine to the respiratory neuron in the medulla.