BEHAVIORAL TREATMENT OF RAYNAUD'S PHENOMENON

在我们目前的调查中，我们证明了患有 特发性雷诺病增加了α-肾上腺素能 与年龄和性别匹配的受体敏感性和/或密度的比较 控制。最近的动物研究表明，局部降温 增强α2受体介导的皮肤血管收缩 血管。我们现在建议确定这种增强作用是否 在特发性雷诺病患者中发生的程度比 在普通人身上。尽管有人提出了遗传病因学 对于雷诺氏病，它从来没有系统地 调查过了。我们建议检查家族性发生的 雷诺正在进行一项对照研究。 使用选择性指神经阻滞和动脉内灌注 心得安，我们发现在体温下血管扩张 反馈是通过β-肾上腺素能机制调节的，而不是 通过传出的指神经。流通领域的作用 儿茶酚胺在反馈诱导的血管扩张中的作用 经过检查，但可以提供一个合理的生理基础 这个机制。我们建议测量循环中的儿茶酚胺 雷诺病患者和正常人的对照研究 人。 在我们研究雷诺氏病的肾上腺素受体的过程中， 我们发现外周血细胞的敏感度和/或密度 血管α和β肾上腺素能受体显著降低 正常女性多于正常男性。考虑到性别差异 在许多血管疾病的发病率中，重要的是 确定这些发现的生理意义以及 它们背后的机制。我们建议研究一下 交感神经系统和月经周期 调节女性的血管肾上腺素能受体。因为我们有 只研究了皮肤肾上腺素受体的性别差异 血管床，我们建议确定我们的发现是否延伸到 肌肉循环也是如此。

In our current investigations, we demonstrated that patients with idiopathic Raynaud's disease have increased alpha-adrenergic receptor sensitivity and/or density compared to age and sex-matched controls. Much recent animal research shows that local cooling potentiates alpha2 receptor mediated vasoconstriction in cutaneous blood vessels. We now propose to determine if this potentiation occurs to a greater extent in idiopathic Raynaud's patients than in normal persons. Although a genetic etiology has been suggested for Raynaud's disease, it has never been systematically investigated. We propose to examine the familial occurrence of Raynaud's in a controlled study. Using selective digital nerve blocks and intra-arterial infusions of propranolol, we found that vasodilation during temperature feedback is mediated-through a beta-adrenergic mechanism and not through efferent digital nerves. The role of circulating catecholamines in feedback-induced vasodilation has never been examined, but could provide a plausible physiological basis for this mechanism. We propose to measure circulating catecholamines in controlled studies of Raynaud's disease patients and normal persons. In the course of our work on adrenoceptors in Raynaud's disease, we discovered that the sensitivity and/or density of peripheral vascular alpha and beta-adrenergic receptors is significantly lower in normal women than in normal men. In light of sex differences in the incidence of many vascular diseases, it is important to determine the physiological significance of these findings and the mechanisms which underlie them. We propose to examine the role of the sympathetic nervous system and the menstrual cycle in modulating vascular adrenergic receptors in women. Since we have only studied sex differences in adrenoceptors in a cutaneous vascular bed, we propose to determine if our findings extend to the muscle circulation as well.