MENSTRUAL PHASE AND NEURAL CONTROL OF SKIN BLOOD FLOW

描述(改编自申请人的摘要)：反射控制 皮肤循环既是体温调节的，也是 非体温调节起源，通过交感血管收缩和 交感神经的主动血管扩张机制。申请人以前曾 表明这两个传出系统中的每一个都受以下控制 体内温度，皮肤温度，运动相关的反射，以及 压力反射。伴随月经各期的类固醇变化 已知循环作为温度调节的背景修饰物 控制皮肤血液流动。PI的工作假设是，在 黄体期，黄体酮通过转变为 更高的内部温度阈值使其启动和升高 对于任何给定的体温，血管收缩活动也一样。高架 排卵期的雌激素水平被假设为 对血管收缩和活性血管扩张剂的方向相反作用 功能。通过选择性局部阻断血管收缩功能 申请者将检查以下方面的主动血管扩张功能的变化 月经期。这种影响将为 有充分记录的基础内部温度和 通过月经周期控制皮肤循环。这个 申请者还将寻找孕激素和雌激素作用的证据。 在这些阶段性变化中，通过利用 卵泡(均为低)、排卵(雌激素升高)、 和黄体期(两者都升高)，以找出这些荷尔蒙模式如何影响 血管扩张剂和血管收缩通路的控制。这些研究 将由对控制的更改进行检查来补充 活动期和安慰剂期之间的血管收缩和血管扩张通路 口服避孕药。申请者将评估外围设备 通过测试这些类固醇在血管运动功能中的作用 控制应用去甲肾上腺素或去甲肾上腺素引起的血管收缩反应 直接应用乙酰胆碱的血管扩张剂反应是依赖的 在月经周期的阶段。这个问题还会更进一步 通过发现皮肤血流量水平在自由的区域是否 自主神经的影响(通过皮肤神经阻滞)和在完好区 神经支配在月经周期的不同阶段或在月经周期的不同阶段之间不同 口服避孕药的使用。前列腺素合成在上皮性高血压中的作用 主动血管扩张系统的体温调节控制的转变将 也要接受评估。

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.