MENSTRUAL PHASE AND NEURAL CONTROL OF SKIN BLOOD FLOW

描述（改编自申请人的摘要）： 皮肤循环既有温度调节作用， 非体温调节起源，通过交感血管收缩剂发生， 交感神经活性血管舒张机制。 申请人此前 显示这两个传出系统中的每一个都受到 内部温度、皮肤温度、运动相关反射，以及 压力感受性反射 伴随月经期的类固醇变化 已知循环作为体温调节的背景调节剂， 控制皮肤血液流动。 PI的工作假设是， 黄体期，孕酮通过转移到一个 启动的内部温度阈值较高， 血管收缩剂的活性。 升高 假设排卵期的雌激素水平 对血管收缩和活性血管舒张剂的方向相反的作用 功能 通过选择性局部阻断血管收缩功能， 申请人将检查主动血管扩张功能的变化， 月经期 这种效应将为 基础内部温度的阶段性变化和 通过月经周期控制皮肤循环。 的 申请人还将寻求证据证明孕酮和雌激素的作用 在这些阶段性的变化，利用正常的波动， 卵泡（均较低）、排卵（雌激素升高） 和黄体（两者都升高）阶段，以了解这些激素模式如何影响 血管扩张和血管收缩途径的控制。 这些研究 将辅之以审查控制 活性阶段和安慰剂阶段之间的血管收缩剂和血管舒张剂通路 口服避孕药。 申请人将评估外围设备 通过测试这些类固醇在血管功能中的作用， 血管收缩反应控制应用去甲肾上腺素或 血管舒张反应直接应用乙酰胆碱是依赖于 月经周期的阶段。 这个问题将进一步 通过发现在没有皮肤的区域中的皮肤血流水平来解决。 自主神经影响（通过皮神经阻滞）和在完整的区域 神经支配在月经周期的各阶段之间或在月经周期的各阶段之间变化。 使用口服避孕药。 前列腺素合成的作用在向上 主动血管扩张系统的温度调节控制的改变将 也被评价。

DESCRIPTION (Adapted from the applicant's abstract): Reflex control of the cutaneous circulation is both of thermoregulatory and of non-thermoregulatory origin and occurs via sympathetic vasoconstrictor and sympathetic active vasodilatory mechanisms. The applicant has previously shown that each of these 2 efferent systems is subject to control by internal temperature, skin temperature, exercise-associated reflexes, and baroreflexes. Steroidal changes accompanying the phases of the menstrual cycle are known to act as background modifiers of the thermoregulatory control of skin blood flow. The PI's working hypothesis is that in the luteal phase, progesterone inhibits active vasodilation by shifting to a higher internal temperature threshold for its initiation and elevates vasoconstrictor activity for any given body temperature as well. Elevated estrogen levels in the ovulatory phase are hypothesized to have directionally opposite effects on vasoconstriction and active vasodilator function. Through selective local blockade of vasoconstrictor function the applicant will examine changes in active vasodilator function among menstrual phases. Such effects would provide mechanisms for the well-documented phasic changes in basal internal temperature and in the control of the cutaneous circulation through the menstrual cycle. The applicant will also seek evidence for the roles of progesterone and estrogen in these phasic changes by taking advantage of the normal fluctuations of steroid levels among follicular (both low), ovulatory (estrogen elevated), and luteal (both elevated) phases to find how those hormonal patterns affect the control of the vasodilator and vasoconstrictor pathways. These studies will be complemented by examinations of alterations in control of the vasoconstrictor and vasodilator pathways between active and placebo phases of oral contraceptives. The applicant will evaluate peripheral contributions by these steroids in vasomotor function by testing whether vasoconstrictor responses to controlled application of norepinephrine or vasodilator responses to direct application of acetylcholine are dependent on the phase of the menstrual cycle. This question will be further addressed by finding if the level of skin blood flow in areas free of autonomic influences (via cutaneous nerve block) and in areas with intact innervation vary among phases of the menstrual cycle or between phases of oral contraceptive use. The role of prostaglandin synthesis in the upward shift of the thermoregulatory control of the active vasodilator system will also be evaluated.