Why the study?
Does rapid, low-level lower body negative pressure (LBNP) cause transient changes in cardiovascular variables in humans?
Does rapid, low-level lower body negative pressure (LBNP) cause transient changes in cardiovascular variables in humans?
Rapid changes in mild LBNP cause significant transient changes in mean arterial pressure, indicating that neural responses affecting total peripheral resistance are not fast enough to compensate.
May affect LBNP protocol design in research; leaves open clinical translation of transient responses.
The hypothesis tested was that there are significant transient changes in the cardiovascular variables after rapid onset and release of mild lower body negative pressure (LBNP, -20 mmHg), even in experimental situations where there is no detectable change in steady-state values. Twelve subjects participated in the study. Heart rate, stroke volume (SV), cardiac output, mean arterial pressure (MAP), total peripheral resistance (TPR), acral and nonacral skin blood flow, and blood flow velocity in the brachial artery were continuously recorded during the pre-LBNP period (0-120 s), during LBNP (120-420 s), and during the post-LBNP period (420-600 s). The main finding was that MAP is transiently but strongly affected by rapid changes in LBNP as small as -20 mmHg. There was also a characteristic asymmetry in cardiovascular responses to the onset and release of LBNP, particularly in the responses in SV. The transient changes in MAP indicate that the neural responses that affect TPR are not fast enough to compensate for the rapid changes in LBNP. In this case, the arterial baroreceptors will be activated as well as the low-pressure baroreceptors that sense central venous pressure. This must be taken into consideration in future discussions of the results of LBNP protocols.
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Hisdal et al. (2001) studied this question.
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