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Updated: Apr 1, 2026

Invasive Hemodynamic Monitoring of Aortic and Pulmonary Artery Hemodynamics in a Large Animal Model of ARDS
Published on: November 26, 2018
Pressure-dependent coupling between arterial pressure and intercostal muscle blood-flow index during acute
Masashi Ichinose1, Mikie Nakabayashi2,3, Yumie Ono4
1Human Integrative Physiology Laboratory, School of Business Administration, Meiji University, Suginami-ku, Tokyo, Japan.
Abstract:
Regulation of respiratory muscle blood flow during acute systemic hypotension remains poorly understood in humans because continuous assessment of microvascular perfusion during rapid haemodynamic transients has been technically challenging. Using diffuse correlation spectroscopy, we investigated second-by-second coupling between mean arterial pressure (MAP) and intercostal muscle blood-flow index (BFI) during an abrupt hypotensive stimulus in healthy humans. Fifteen young men underwent 5 min of suprasystolic bilateral thigh occlusion followed by rapid cuff release. The MAP and intercostal BFI were analysed at 1 Hz over drop (0-10 s) and recovery (10-20 s) phases. Phase-specific MAP-BFI gain (%BFI per 1% change in MAP) was estimated using linear mixed-effects models, with within-participant centring. Immediately after cuff release, MAP and BFI decreased almost concomitantly, reached nadirs at ∼10 s and recovered towards baseline within the next ∼10 s. Phase-averaged reductions in BFI were associated with reductions in MAP during the drop phase (Pearson's r = 0.66, P = 0.00701). Mixed-effects modelling revealed near-unity MAP-BFI gain in both phases (drop, 0.89 [95% confidence interval 0.63-1.15], P < 0.001 vs. 0, P = 0.417 vs. 1; recovery, 0.95 [0.50-1.40], P < 0.001 vs. 0, P = 0.830 vs. 1), with no phase difference (recovery-drop = 0.06 [-0.46 to 0.58], P = 0.824). Individual-level gains showed greater variability, particularly during recovery. These findings demonstrate tight pressure-BFI coupling over seconds-long time scales, indicating that perfusion pressure is a key determinant of intercostal microvascular blood-flow dynamics during acute hypotensive stress.
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