Coward D M
Department of Clinical Research & Development, Sandoz Pharma Ltd., Basel, Switzerland.
Neurology. 1994 Nov;44(11 Suppl 9):S6-10; discussion S10-1.
Pharmacologic and electrophysiologic studies over the past 20 years have shown tizanidine to be a potent, central-acting myotonolytic agent that principally affects spinal polysynaptic reflexes. This action arises from agonistic activity of the compound at noradrenergic alpha 2 receptors, resulting in both direct impairment of excitatory amino acid release from spinal interneurons and a concomitant inhibition of facilitatory coeruleospinal pathways. Similar alpha 2-receptor-mediated inhibition of interneuronal activity appears to underlie the additional antinociceptive and anticonvulsant activity of tizanidine reported in several species and test paradigms. Despite its structural and biochemical similarity to clonidine, the cardiovscular properties of tizanidine are mild and transitory in relation to its activity as a muscle relaxant. These findings, together with a possible greater separation between myotonolytic and general CNS depressant activity than with other agents, make tizanidine a valuable addition in the pharmacologic treatment of spasticity.
过去20年的药理学和电生理学研究表明,替扎尼定是一种强效的中枢性肌松剂,主要影响脊髓多突触反射。这种作用源于该化合物对去甲肾上腺素能α2受体的激动活性,导致脊髓中间神经元兴奋性氨基酸释放直接受损,并同时抑制易化性蓝斑脊髓通路。在几个物种和试验范式中报道的替扎尼定的额外镇痛和抗惊厥活性似乎也基于类似的α2受体介导的中间神经元活动抑制。尽管替扎尼定在结构和生化方面与可乐定相似,但其作为肌肉松弛剂的活性相关的心血管特性轻微且短暂。这些发现,以及与其他药物相比,替扎尼定的肌松活性和一般中枢神经系统抑制活性之间可能有更大的差异,使得替扎尼定成为痉挛药物治疗中有价值的补充药物。