Scherrer U, Vissing S F, Victor R G
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-9034.
Circulation. 1988 Jul;78(1):49-59. doi: 10.1161/01.cir.78.1.49.
Although previous studies in both animals and humans have suggested that cardiac baroreceptors modulate reflex sympathetic vasoconstriction during exercise, more recent studies in conscious animals have not supported this view. To further test this concept in humans, we measured sympathetic nerve discharge with intraneural microelectrodes while we used static handgrip to activate the exercise pressor reflex and nonhypotensive lower-body negative pressure (LBNP) to selectively unload the cardiac baroreflex. In nine healthy subjects, we measured blood pressure, heart rate, central venous pressure, and muscle sympathetic nerve activity (MSNA) from the peroneal nerve (resting leg) during 2 minutes of static handgrip at 20% and 30% of maximal voluntary contraction (MVC) alone and in combination with LBNP at -5 mm Hg. Handgrip alone (exercise reflex) at 20% and 30% MVC caused graded increases in MSNA. LBNP alone (cardiac reflex) did not alter blood pressure or heart rate but decreased central venous pressure by 2.5 +/- 0.1 mm Hg (mean +/- SEM, p less than 0.05) and increased MSNA by 92 +/- 22% over the control value. Most important, handgrip performed during LBNP (interaction of reflexes) caused increases in MSNA that were comparable with the increases during handgrip alone: +114 +/- 32% versus +175 +/- 89% at 20% MVC and +328 +/- 101% versus +431 +/- 110% at 30% MVC (handgrip plus LBNP vs. handgrip alone, p greater than 0.1). Pressor and heart rate responses to handgrip also were unaffected by LBNP. In five additional experiments, comparable findings were obtained when the LBNP was superimposed on handgrip rather than handgrip being superimposed on LBNP. In conclusion, this study provides direct evidence in humans that nonhypotensive LBNP does not augment muscle sympathetic outflow during static handgrip and challenges the concept of an important interaction between cardiac baroreceptor and exercise pressor reflexes during this form of exercise.
尽管先前在动物和人类身上进行的研究表明，心脏压力感受器在运动过程中调节反射性交感神经血管收缩，但最近在清醒动物身上进行的研究并不支持这一观点。为了在人类中进一步验证这一概念，我们使用神经内微电极测量交感神经放电，同时使用静态握力来激活运动升压反射，并使用非低血压性下肢负压（LBNP）来选择性地卸载心脏压力反射。在9名健康受试者中，我们在单独进行20%和30%最大自主收缩（MVC）的静态握力以及与-5 mmHg的LBNP联合进行2分钟静态握力过程中，测量了腓总神经（静息腿）的血压、心率、中心静脉压和肌肉交感神经活动（MSNA）。单独的握力（运动反射）在20%和30%MVC时导致MSNA分级增加。单独的LBNP（心脏反射）并未改变血压或心率，但使中心静脉压降低了2.5±0.1 mmHg（平均值±标准误，p<0.05），并使MSNA比对照值增加了92±22%。最重要的是，在LBNP期间进行的握力（反射相互作用）导致MSNA的增加与单独握力时的增加相当：在20%MVC时为+114±32%对+175±89%，在30%MVC时为+328±101%对+431±110%（握力加LBNP对单独握力，p>0.1）。对握力的升压和心率反应也不受LBNP影响。在另外5个实验中，当LBNP叠加在握力上而不是握力叠加在LBNP上时，也获得了类似的结果。总之，本研究为人类提供了直接证据，即非低血压性LBNP在静态握力期间不会增加肌肉交感神经流出，并对这种运动形式下心脏压力感受器与运动升压反射之间重要相互作用的概念提出了挑战。
