BEHAVIORAL TREATMENT OF RAYNAUD'S PHENOMENON

在我们目前的调查中，我们首先证实， 雷诺氏病患者报告的温度引起的症状减轻 温度反馈（TEMP）和冷胁迫下的温度反馈（TEMPCS）。 维持了3年的随访期，TEMPCS组 保持了对TEMP组的优势。 然后我们证明了， β-肾上腺素能血管舒张机制在温度期间是活跃的， 反馈和毛细血管血流量显着增加， 患者的反馈，而不是正常人。 我们现在建议确定是否有 温度反馈的影响是神经介导的，看看是否 这些影响普遍适用于下肢，并确定是否 增加毛细血管血流量是造成长期影响的原因， TEMP和TEMPCS治疗以及后者的持续优越性。 如果TEMPCS治疗促进毛细血管血流量增加， 时间段，它可能是有益的雷诺现象的治疗 在硬皮病中。 我们建议在对照研究中测试这一点，使用 在过去一年中执行了同位素清除程序。 最近，有报道称， 特发性雷诺病患者的血小板。 因此， 建议检查手指血管对动脉灌注的反应， 可乐定，选择性α 2激动剂。 此外，有证据表明， 从交感神经末梢释放的去甲肾上腺素（NE）可产生 与外源性给药不同的血管效应 儿茶酚胺或合成激动剂。 酪胺通过释放储存的 NE从肾上腺素能神经末梢，我们建议比较数字 雷诺病患者和匹配的患者对酪胺的血管反应 正常人 最后，关于雷诺氏病病因的研究已经 由于无法在实验室中制造攻击而受阻。 最近， Wise等人报告了14例雷诺氏病患者中100%诱发发作 使用全身冷却。 我们建议采用这一程序， 交感神经在血管痉挛发作中的作用 手指神经阻滞

In our current investigations we first verified that the significant symptom reductions reported by Raynaud's disease patients given temperature feedback (TEMP) and temperature feedback under cold stress (TEMPCS) were maintained over a 3-year, follow-up period and that the TEMPCS group maintained its superiority over the TEMP group. We then demonstrated that a beta-adrenergic vasodilating mechanism is active during temperature feedback and that capillary blood flow is significantly increased during feedback in patients but not normals. We now propose to determine if any of the effects of temperature feedback are neurally mediated, to see if these effects generalize to the lower extremities, and to determine if increased capillary blood flow is responsible for the long-term effects of TEMP and TEMPCS treatment and for the continued superiority of the latter. If TEMPCS treatment promotes increased capillary blood flow over extended time periods, it may be beneficial in the treatment of Raynaud's phenomenon in scleroderma. We propose to test this in a controlled study, using an isotope clearance procedure implemented during the past year. Recently, an increased number of Alpha2 receptors has been reported on the platelets of patients with idiopathic Raynaud's disease. We, therefore, propose to examine finger vascular responses to arterial infusion of clonidine, a selective Alpha2 agonist. Also, evidence exists that norepinephrine (NE) released from sympathetic nerve endings may produce vascular effects different from those of exogenously administered catecholamines or synthetic agonists. Tyramine acts by liberating stored NE from adrenergic nerve endings and we propose to compare the digital vascular responses to tyramine of Raynaud's disease patients and matched normals. Finally, research on the etiology of Raynaud's disease has been hindered by the inability to produce attacks in the laboratory. Recently, Wise et al. reported induction of attacks in 100% of 14 Raynaud's patients using total body cooling. We propose to employ this procedure to examine the role of the sympathetic nerves in vasospastic attacks using selective digital nerve blocks.