What is the clinical evidence from this study?

Study design: Other. Population: Healthy (n=19). Intervention: Lower body negative pressure (LBNP) vs. Baseline. Primary outcome: Transient changes in systolic and diastolic blood pressure at the onset of LBNP.

December 13, 2008AJP Heart and Circulatory Physiology53 citations

Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

QFQi Fu SSShigeki Shibata JHJeffrey L. Hastings

Key Result

Application of low levels of lower body negative pressure (-10 and -15 mmHg) caused transient reductions in blood pressure that were restored after approximately 15 heartbeats, indicating arterial baroreceptor unloading.

PICO

Population

19 healthy non-athletic adults aged 20 to 54 years underwent lower body negative pressure testing to evaluate hemodynamic responses.

Intervention / Comparator

Lower body negative pressure (LBNP) vs Baseline (-5 to -30 mmHg)

Primary Outcome

Transient changes in systolic and diastolic blood pressure at the onset of LBNP

Limitations

Arterial pressure was measured noninvasively and indirectly with Portapres, which may not perfectly reflect true central arterial pressure.
Beat-by-beat hemodynamic variables were derived from the Modelflow method rather than gold-standard invasive methods.

Abstract

Low levels (i.e., </=20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload "selectively" cardiopulmonary baroreceptors in humans, since steady-state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20-54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan-Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and -15- and -30-mmHg LBNP for 6 min each. Application of -15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after approximately 15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at -5- and in all at -10-mmHg LBNP. The delay for left ventricular stroke volume to fall at -15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during -15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at -30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., -10 and -15 mmHg) of LBNP in humans. Thus "selective" unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.

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