Sequential Modulation of Cardiac Autonomic Control Induced by Cardiopulmonary and Arterial Baroreflex Mechanisms

Abstract

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 Hg. 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 (α 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 α 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 (LF R-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 LF R-R , which precedes the changes in the hemodynamics and in the indexes of arterial baroreflex control.