Kimmerly D S, Shoemaker J K
Neurovascular Research Laboratory, School of Kinesiology, University of Western Ontario, London, N6A 3K7 Ontario, Canada.
Am J Physiol Heart Circ Physiol. 2003 Apr;284(4):H1198-204. doi: 10.1152/ajpheart.00229.2002. Epub 2002 Dec 19.
We previously demonstrated that diuretic-induced hypovolemia resulted in an enhanced baroreflex-mediated increase in integrated muscle sympathetic nerve activity (MSNA) and vasomotor tone during lower body negative pressure (LBNP) (Am J Physiol Heart Circ Physiol 282: H645-H655, 2002). The purpose of this study was to perform a retrospective analysis of these data and examine the ability of relative MSNA burst amplitude distributions to highlight differences in baseline sympathetic nerve discharge patterns. An additional purpose was to determine whether differential responses in MSNA burst frequency and burst amplitude affect conclusions regarding sympathetic reflex control. MSNA, stroke volume (SV, Doppler), and estimated central venous pressure (CVP, dependent arm technique) were measured during LBNP within the placebo (Normo) and diuretic (Hypo; 100 mg/day spironolactone for 3 days) conditions (n = 8). Compared with Normo, MSNA burst frequency at rest was elevated, and there was a rightward shift in the median of the relative burst amplitude distribution (P < 0.05) in Hypo. During LBNP, the larger rise in total MSNA during Hypo versus Normo was due to greater increases in relative burst amplitude with no difference in the burst frequency response. The MSNA burst frequency response to LBNP was shifted to a higher position on the same MSNA-CVP curve during Hypo compared with Normo. In contrast, the Hypo burst amplitude response was shifted to a new curve with a slope that was similar to the Normo relationship. These data support the use of probability distribution analysis to examine intraindividual differences in baseline and reflex-mediated increases in MSNA burst amplitude. Furthermore, the differential effect of hypovolemia on the responses of burst frequency and amplitude during graded LBNP suggests that burst frequency data alone may not adequately represent reflex control of sympathetic outflow.
我们之前证明，在下肢负压（LBNP）期间，利尿剂诱导的血容量减少导致压力反射介导的肌肉交感神经活动（MSNA）积分和血管运动张力增强（《美国生理学杂志：心脏和循环生理学》282：H645 - H655，2002）。本研究的目的是对这些数据进行回顾性分析，并检验相对MSNA爆发幅度分布突出基线交感神经放电模式差异的能力。另一个目的是确定MSNA爆发频率和爆发幅度的差异反应是否会影响关于交感反射控制的结论。在安慰剂（正常组）和利尿剂（低血容量组；100毫克/天螺内酯，持续3天）条件下进行LBNP时，测量了MSNA、每搏输出量（SV，多普勒法）和估计中心静脉压（CVP，依赖臂技术）（n = 8）。与正常组相比，低血容量组静息时的MSNA爆发频率升高，相对爆发幅度分布的中位数向右偏移（P < 0.05）。在LBNP期间，低血容量组与正常组相比，总MSNA的更大升高是由于相对爆发幅度的更大增加，爆发频率反应无差异。与正常组相比，低血容量组对LBNP的MSNA爆发频率反应在相同的MSNA - CVP曲线上移至更高位置。相反，低血容量组的爆发幅度反应移至一条斜率与正常组关系相似的新曲线上。这些数据支持使用概率分布分析来检查MSNA爆发幅度基线和反射介导增加的个体内差异。此外，血容量减少对分级LBNP期间爆发频率和幅度反应的差异效应表明，仅爆发频率数据可能无法充分代表交感神经流出的反射控制。
