BEHAVIORAL TREATMENT OF RAYNAUD'S PHENOMENON

在我们目前的调查中，我们首先证实了 雷诺病患者在发热后症状减轻的报告 温度反馈(Temp)和冷应激温度反馈(TEMPCS) 维持了3年的随访期，TEMPCS小组 保持了对临时组的优势。然后我们展示了这一点 一种β-肾上腺素能的血管扩张机制在温度下是活跃的 反馈和毛细血管血流量显著增加 对病人的反馈，而不是正常人的反馈。我们现在建议确定是否有 温度反馈的影响是由神经调节的，以了解 这些影响推广到下肢，并确定是否 毛细血管血流量增加是高血压长期影响的原因 TEMP和TEMPCS的治疗，以及后者的持续优势。 如果TEMPCS治疗在延长时间内促进毛细血管血流增加 时间段，对雷诺现象的治疗可能是有益的 硬皮病。我们建议在一项对照研究中测试这一点，使用 在过去一年中实施了同位素清除程序。 最近，有报道称α2受体的数量增加了。 特发性雷诺病患者的血小板。因此，我们， 建议检查手指血管对动脉输注的反应 可乐定，一种选择性的α2激动剂。此外，有证据表明， 交感神经末梢释放的去甲肾上腺素(NE)可产生 血管效应与外源性给药不同 儿茶酚胺或合成激动剂。酪胺通过释放储存的 NE来自肾上腺素能神经末梢，我们建议将数字 雷诺病患者及配对患者对酪胺的血管反应 法线。最后，对雷诺病的病因学进行了研究 由于无法在实验室中制造攻击而受到阻碍。最近， Wise等人。据报道，在14名雷诺氏病患者中100%发生了发作 使用全身降温。我们建议采用这一程序来检查 交感神经在选择性血管痉挛发作中的作用 数字神经阻滞。

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.