Key result
Incremental LBNP suppresses systemic hemodynamics via preload reduction, reversing fully within three respiratory cycles upon release.
Why the study?
The exact hemodynamic mechanisms of graded lower body negative pressure and its abrupt release have not been characterized in detail, limiting its potential applications in humans.
Does incremental lower body negative pressure and its abrupt release alter left ventricular hemodynamics in anesthetized pigs?
Does incremental lower body negative pressure and its abrupt release alter left ventricular hemodynamics in anesthetized pigs?
Answers are grounded in this paper and cite their sources.
Incremental lower body negative pressure induces reversible, preload-dependent depression of systemic hemodynamics in a porcine model, providing translational insights for human applications like spaceflight countermeasures.
Lower body negative pressure (LBNP) has been implemented as a tool to simulate systemic effects of hypovolemia, understand orthostatic challenges and study G load stress in humans. However, the exact hemodynamic mechanisms of graded LBNP followed by its abrupt release have not been characterized in detail, limiting its potential applications in humans. Here, we set out to investigate the immediate hemodynamic alterations occurring during LBNP in healthy Landrace pigs. Invasive cardiac monitoring via extensive pressure volume loop analysis was carried out during application of incremental LBNP up to life threatening levels from -15 to -45 mmHg as well as during its abrupt release. Three different sealing positions were evaluated. Incremental LBNP consistently induced a preload dependent depression of systemic hemodynamics according to the Frank-Starling mechanism. Overall, the pressure-volume loop progressively shifted leftwards and downwards with increasing LBNP intensity. The abrupt release of LBNP reverted the above-described hemodynamic changes to baseline values within only three respiratory cycles. These data provide quantitative translational insights into hemodynamic mechanisms of incremental and very high levels of LBNP, levels of seal and effect of abrupt release for future human applications, such as countermeasure development for long spaceflight.
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Zirngast et al. (2022) studied Healthy (animal model) (n=9). Lower body negative pressure (LBNP) vs. Baseline was evaluated on Left ventricular hemodynamics (pressure-volume loop changes). Incremental lower body negative pressure induced a preload-dependent depression of systemic hemodynamics, shifting the pressure-volume loop leftwards and downwards, which was fully reversed within three respiratory cycles upon abrupt release.
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