Sequential modulation of cardiac autonomic control induced by cardiopulmonary and arterial baroreflex mechanisms

Background-Nonhypotensive lower body negative pressure (LBNP) induces a reflex increase in forearm vascular resistance and muscle sympathetic neural discharge without affecting mean heart rate. We tested the hypothesis that a reflex change of the autonomic modulation of heartbeat might arise during low intensity LBNP without changes of mean heart rate. Methods and Results-Ten healthy volunteers underwent plasma catecholamine evaluation and a continuous recording of ECG. finger blood pressure, respiratory activity, and central venous pressure (CVP) during increasing levels of LBNP up to -40 mm Fig. Spectrum and cross-spectrum analyses assessed the changes in the spontaneous variability of R-R interval, respiration, systolic arterial pressure (SAP), and CVP and in the gain (alpha (LF)) of arterial baroreflex control of heart rate. Baroreceptor sensitivity was also evaluated by the SAP/R-R spontaneous sequences technique, LBNP began decreasing significantly: CVP at -10, R-R interval at -20, SAP at -40, and the indexes alpha (LF) and baroreceptor sensitivity at -30 and -20 mm Hg, compared with baseline conditions. Plasma norepinephrine increased significantly at -20 mm Hg. The normalized low-frequency component of R-R variability (LFR.R) progressively increased and was significantly higher than in the control condition at - 15 mm Hg. Conclusions-Nonhypotensive LBNP elicits a reflex increase of cardiac sympathetic modulation, as evaluated by LFR.R, which precedes the changes in the hemodynamics and in the indexes of arterial baroreflex control.