TY - JOUR
T1 - Sequential modulation of cardiac autonomic control induced by cardiopulmonary and arterial baroreflex mechanisms
AU - Furlan, Raffaello
AU - Jacob, Giris
AU - Palazzolo, Laura
AU - Rimoldi, Alexandra
AU - Diedrich, Andre
AU - Harris, Paul A.
AU - Porta, Alberto
AU - Malliani, Alberto
AU - Mosqueda-Garcia, Rogelio
AU - Robertson, David
PY - 2001/12/11
Y1 - 2001/12/11
N2 - 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 (αLF) 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 (αLF) 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.
AB - 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 (αLF) 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 (αLF) 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.
KW - Baroreceptors
KW - Hemodynamics
KW - Nervous system, sympathetic
KW - Pressure
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M3 - Article
C2 - 11739308
AN - SCOPUS:0035846551
SN - 0009-7322
VL - 104
SP - 2932
EP - 2937
JO - Circulation
JF - Circulation
IS - 24
ER -