BEHAVIORAL TREATMENT OF RAYNAUD'S PHENOMENON

在我们目前的研究中，我们证明， 特发性雷诺病具有增加α-肾上腺素能 与年龄和性别匹配的受体敏感性和/或密度相比 对照 最近的许多动物研究表明，局部降温 增强α 2受体介导的皮肤血管收缩 血管 我们现在要确定这种增强作用 在特发性雷诺氏病患者中发生的程度大于 在正常人身上。 尽管有人认为是遗传病因 对于雷诺氏病， 研究了 我们建议检查家族性的发生， 雷诺在进行对照研究 使用选择性手指神经阻滞和动脉内灌注 普萘洛尔，我们发现， 反馈是通过β-肾上腺素能机制介导的， 通过传出指神经。 循环的作用 反馈诱导的血管舒张中的儿茶酚胺从未被 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 在雷诺病患者和正常人的对照研究中， 人士 在我们研究雷诺氏病中肾上腺素受体的过程中， 我们发现外周血淋巴细胞的敏感性和/或密度 血管α和β肾上腺素能受体显著降低 在正常女性中的比例要比在正常男性中的比例高。 鉴于性别差异 在许多血管疾病的发病率中， 确定这些发现的生理意义， 它们背后的机制。 我们建议研究 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。 既然我们有 只研究了皮肤组织中肾上腺素受体的性别差异， 血管床，我们建议确定我们的研究结果是否延伸到血管床。 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.