Potts J T, Shi X, Raven P B
Department of Physiology, Texas College of Osteopathic Medicine, Fort Worth 76107, USA.
Am J Physiol. 1995 Apr;268(4 Pt 2):H1567-76. doi: 10.1152/ajpheart.1995.268.4.H1567.
Numerous studies have reported that, at rest, maximal carotid baroreflex gain is modulated by cardiopulmonary baroreceptors. The purpose of this study was to measure the maximal gain for carotid baroreflex control of heart rate (HR) and blood pressure [mean arterial pressure (MAP)] during dynamic exercise alone and when exercise was accompanied by two levels of cardiopulmonary baroreceptor unloading. Lower body negative pressure (LBNP) produced similar reductions in central venous pressure (CVP) at rest and during exercise. Baroreflex gain for HR at rest was not affected by low-level LBNP but was significantly increased by high-level LBNP [-0.31 +/- 0.05 to -0.57 +/- 0.23 beats.min-1.mmHg-1 carotid sinus pressure (CSP), no LBNP vs. high-level LBNP, P < 0.05]. Exercise combined with low- and high-level LBNP resulted in reflex HR gains (-0.83 +/- 0.44 and -0.83 +/- 0.17 beats.min-1.mmHg-1 CSP, low- vs. high-level LBNP, P < 0.05) that were significantly greater than the algebraic sum of the HR gain measured during exercise and LBNP alone. Neither exercise nor the two levels of LBNP significantly altered baroreflex gain for MAP. The slope relating HR gain to CVP at rest was significant (0.07 +/- 0.02 beats.min-1.mmHg CSP-1.mmHg CVP-1, P < 0.01) and increased 114% during exercise (P < 0.05). A similar analysis of MAP gain found no difference in slope between rest and exercise (P > 0.05). Together these data indicate 1) a tonic inhibitory interaction between cardiopulmonary baroreceptors and carotid baroreflex control of HR during exercise, and 2) a nonlinear relationship between deactivation of cardiopulmonary baroreceptors and changes in carotid baroreflex gain. This interaction may improve overall cardiovascular regulation when central blood volume and/or CVP is reduced, as has been reported during prolonged exercise in the heat.
大量研究报告称，在静息状态下，最大颈动脉压力反射增益受心肺压力感受器调节。本研究的目的是测量单独进行动态运动时以及运动伴有两种水平的心肺压力感受器卸载时，颈动脉压力反射对心率（HR）和血压[平均动脉压（MAP）]的最大增益。下体负压（LBNP）在静息和运动时产生相似程度的中心静脉压（CVP）降低。静息时HR的压力反射增益不受低水平LBNP影响，但受高水平LBNP显著增加[-0.31±0.05至-0.57±0.23次·分钟-1·mmHg-1颈动脉窦压力（CSP），无LBNP与高水平LBNP相比，P<0.05]。运动与低水平和高水平LBNP相结合导致反射性HR增益（-0.83±0.44和-0.83±0.17次·分钟-1·mmHg-1 CSP，低水平与高水平LBNP相比，P<0.05）显著大于单独运动和LBNP时测量的HR增益的代数和。运动和两种水平的LBNP均未显著改变MAP的压力反射增益。静息时将HR增益与CVP相关的斜率显著（0.07±0.02次·分钟-1·mmHg CSP-1·mmHg CVP-1，P<0.01），运动时增加114%（P<0.05）。对MAP增益的类似分析发现静息和运动时斜率无差异（P>0.05）。这些数据共同表明：1）运动期间心肺压力感受器与颈动脉压力反射对HR的控制之间存在紧张性抑制相互作用；2）心肺压力感受器失活与颈动脉压力反射增益变化之间存在非线性关系。当中心血容量和/或CVP降低时，如在热环境中长时间运动时所报道的那样，这种相互作用可能会改善整体心血管调节。
