INFLUENCE OF PULSATILE PRESSURE ON THE BAROREFLEX

平均动脉压升高会增加压力感受器 反射性抑制交感神经活动和缓冲的活动 压力的上升。在体内，压力感受器暴露在 脉动压力，可通过改变压力反射 单位时间的压力感受器活动量，模式 活动度和/或反射的适应速度 持续的压力感受器刺激。 交感神经抑制的幅度和选择性可能不会 仅是单位压力感受器活动量的函数 时间，但可以是活动的阶段模式的函数。这个 第一个具体目标是确定和对比 压力感受器对压力感受器的静态和搏动性兴奋 同样水平的压力感受器活动。第二个目标是 确定压力感受器活动/单位的相对影响 时间、活动/单位时间的突发数、活动/突发和 压力感受器反射的瞬时活动峰值。第三个目标是 确定压力感受器激活模式对 反射的区域选择性。 “适应”的规模和选择性，即逃避 持续压力感受性反射抑制引起的交感神经活动 压力的增加，可能取决于 刺激，因此在脉动压力期间改变。第四次 目的是刻画和研究导致 压力感受器在静息和搏动中的适应 压力。第五个目标是确定“中心”的作用 正常血压在静压和脉动压力下的“适应性” 和高血压动物。 为了达到这些目的，麻醉状态下分离的颈动脉窦 狗将暴露在受控水平的静态和脉动 颈动脉窦内径、压力感受器活动和 测量传出交感神经活动。同时进行 传入和传出活动的记录以及同步 两个传出活动的录音将使 压力感受器活动的模式和区域选择性 要评估的响应。电刺激传入神经 还将进行纤维检查，以检查 搏动性。 结果应该定义 压力感受器活动的阶段性及其调节作用 以特定和选择性的方式进行自主控制。结果是 可能对循环系统有重要的影响 高血压等疾病。

An increased mean arterial pressure increases baroreceptor activity which reflexly inhibits sympathetic activity and buffers the rise in pressure. In vivo, the baroreceptors are exposed to a pulsatile pressure that may modify the baroreflex by altering the amount of baroreceptor activity per unit time, the pattern of activity, and/or the rate of adaptation of the reflex during sustained baroreceptor stimulation. The magnitude and selectively of sympathetic inhibition may not only be a function of the amount of baroreceptor activity per unit time but may be a function of the phasic pattern of activity. The first specific aim is to determine and contrast the effects of static and pulsatile activation of baroreceptors on the baroreflex for the same level of baroreceptor activity. The second aim is to determine the relative influence of baroreceptor activity/unit time, number of bursts of activity/unit time, activity/burst, and peak instantaneous activity on the baroreflex. The third aim is to determine the effect of the pattern of baroreceptor activation on the regional selectivity of the reflex. The magnitude and selectivity of "adaptation", i.e. the escape of sympathetic activity from baroreflex inhibition during a sustained increase in pressure, may be dependent on the pattern of stimulation and thus altered during pulsatile pressure. The fourth aim is to characterize and examine the mechanism responsible for the adaptation of baroreceptors during static and pulsatile pressure. The fifth aim is to determine the role of "central adaptation" during static and pulsatile pressure in normotensive and hypertensive animals. To achieve these goals the isolated carotid sinuses in anesthetized dogs will be exposed to controlled levels of static and pulsatile pressure while carotid sinus diameter, baroreceptor activity, and efferent sympathetic activity are measured. Simultaneous recordings of afferent and efferent activity and simultaneous recordings of two efferent activities will enable the role of the pattern of baroreceptor activity and the regional selectivity of the responses to be evaluated. Electrical stimulation of afferent fibers will also be performed to examine central effects of pulsatility. The results should define the functional significance of the phasicity of baroreceptor activity and its role in adjusting autonomic control in a specific and selective way. The results may have important implications pertaining to circulatory disorders such as hypertension.