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帕金森氏病是由于黑包纹状体的含多巴胺的神经细胞变性所引起的。左旋多巴对本病的作用是依赖剩余的黑色纹状休神经细胞由左旋多巴合成多巴胺的能力,并激发纹状体的多巴胺受体。纹状体的多巴胺受体分为2组:一组是与腺苷酸环化酶有关的D-1受体。另一组是与之无关的D-2受体,在治疗中,有时会出现左旋多巴疗效减退以及症状波动现象。这主要是由于黑色纹状体多巴胺神经细胞的进行性变性或纹状体多巴胺受体敏感性降低的原因。对左旋多巴疗效减退的患者,改用多巴胺激动剂可以奏效,因为这类药物具有直接激发纹状体多巴胺受体的作用。抗震颤作用
Parkinson’s disease is caused by the denaturation of dopamine-containing nerve cells in the black striatum. The effect of levodopa on this disease is dependent on the ability of the remaining black striatal Hugh neurons to synthesize dopamine from levodopa and to stimulate the striatum’s dopamine receptors. The striatum dopamine receptors are divided into two groups: one group is the D-1 receptor involved in adenylate cyclase. The other group is a non-related D-2 receptor, in the treatment, sometimes appear levodopa diminished efficacy and symptoms of fluctuations. This is mainly due to progressive degeneration of black striatal dopamine neurons or decreased striatal dopamine receptor sensitivity. In patients with diminished efficacy of levodopa, the switch to dopamine agonists works because these drugs have a direct effect on striatal dopamine receptors. Anti-tremor effect