Lateralized cerebral arterial blood flow and blood pressure adaptations to short-term head-down tilt: a 4D flow MRI
Huan-Ran Hou1, Ting-Ting Zhang1, Ya-Wen Liu1
1Department of Radiology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
Background:
Simulated microgravity, modeled by head-down tilt (HDT), induces cephalad fluid shifts that perturb intracranial hemodynamics and may affect cognitive function. However, the temporal adaptation of cerebral arterial blood flow (CaBF), both during simulated microgravity and throughout the recovery phase, remains incompletely understood.
Methods:
In this study, 38 healthy male participants underwent a 7-day -6° HDT protocol followed by a 5-day recovery phase. Four-dimensional flow magnetic resonance imaging (4D flow MRI) was performed at 8 time points [baseline, HDT 12 h, HDT 1 d, HDT 3 d, HDT 7 d, recovery (R) 1 d, R 3 d, and R 5 d] to quantify CaBF and total cerebral blood inflow (TCBI) in the basilar artery (BA), left and right internal carotid arteries (ICAL and ICAR), and left and right middle cerebral arteries (MCAL and MCAR). Systemic vitals and fasting cortisol/renin were collected, and a computerized reaching task assessed reaction time (RT), movement time (MT), and peak velocity (PV). Time effects were tested with repeated-measures analysis of variance (RM ANOVA) or the Friedman test. Predictors of ≥10% TCBI decrease during HDT and ≥10% TCBI increase during the recovery phase were assessed using logistic regression, and flow-behavior associations were examined using Spearman correlation.
Results:
No significant vessel lumen area changes were found after post-hoc analysis, despite an overall difference observed in the MCAR (χ²=17.40, P=0.015). However, average blood flow significantly changed in the ICAL (χ²=34.16, P<0.001), MCAL (χ²=73.11, P<0.001), and MCAR (χ²=49.02, P<0.001), while BA was stable (RM ANOVA F=0.787, P=0.599) and ICAR showed no significant pairwise effects despite an overall difference (χ²=16.35, P=0.022). TCBI progressively declined during HDT and rebounded rapidly at the onset of recovery (P<0.001). Logistic regression identified systolic blood pressure (SBP) as an independent predictor of a ≥10% TCBI reduction during HDT [P=0.044, odds ratio (OR)=3.004, 95% confidence interval (CI) 1.028-8.777], and baseline cortisol levels predicted significant TCBI decreases from baseline to HDT 7 d (P=0.047, OR=1.306, 95% CI 1.004-1.699). Cognitive-motor testing further revealed phase-dependent changes, with RT and MT generally shortening, most consistently in the no-beep condition, while PV remained stable with beep but increased without beep. Apart from an exploratory negative correlation between TCBI rebound and cued PV (r=-0.360, P=0.031), TCBI changes were largely decoupled from behavioral outcomes.
Conclusions:
This study demonstrates vessel-specific, lateralized adaptation of cerebral arterial inflow during 7 days of -6° HDT and 5 days of recovery, with anterior circulation more responsive to posture-induced fluid shifts and TCBI gradually decreasing then rapidly rebounding after re-ambulation. Interindividual TCBI susceptibility reflects blood pressure and endocrine status, while cognitive-motor changes remain weakly coupled, underscoring the importance of incorporating early-recovery assessments into HDT studies to better characterize cerebrovascular readaptation after re-ambulation.
Clinical Trials Registry:
ChiCTR2500096128.


