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长期以来被认为交感神经系统在偏头痛发病中起重要作用。颅内外血管有着来自上颈节丰富的交感神经支配。当这些神经受刺激后,神经末稍释放去甲肾上腺素作用于α和β受体。偏头痛发作的先驱症状如瞳孔散大、心动过速、焦虑、面色苍白、呼吸急促和局部神经系统症状,是继发于局灶性血管收缩,由儿茶酚胺释放所引起。血浆中CAMP水平被认为是儿茶酚胺系统功能紧张程度的直接指标。多巴胺β羟化酶(DBH)是使多巴胺转化成去甲肾上腺素的一种酶。有人报告在偏头痛发作期血浆DBH是增加的,也有报告用β阻滞剂通过儿茶酚胺系统有予防偏头痛的作用。作者研究了α-2兴奋剂Clonidine和α-2阻滞剂Mianserine对组织胺诱发偏头痛或自发性偏头痛
The sympathetic nervous system has long been thought to play an important role in the pathogenesis of migraine. Intracranial vessels have a rich sympathetic innervation from the upper cervical segment. When these nerves are stimulated, the nerve endings release norepinephrine for the alpha and beta receptors. Preamble migraine attacks such as mydriasis, tachycardia, anxiety, pale, shortness of breath and local nervous system symptoms are secondary to focal vasoconstriction caused by the release of catecholamines. Plasma CAMP levels are thought to be a direct indicator of the magnitude of functional catecholaminergic dysfunction. Dopamine β-hydroxylase (DBH) is an enzyme that converts dopamine to norepinephrine. It has been reported that plasma DBH is increased during migraine attacks and there is also a report of a pro-migraine effect through beta-blockers through the catecholamine system. The authors studied the effects of Clonidine, an alpha-2 agonist, and Mianserine, an alpha-2 blocker, on histamine-induced migraine or spontaneous migraine