Dry immersion (DI) is used to simulate weightlessness. We investigated in healthy volunteers if DI induces changes in ONSD, as a surrogate marker of intracranial pressure (ICP) and how these changes could affect cerebral autoregulation (CA). Changes in ICP were indirectly measured by changes in optic nerve sheath diameter (ONSD). 12 healthy male volunteers underwent 3 days of DI. ONSD was indirectly assessed by ocular ultrasonography. Cerebral blood flow velocity (CBFV) of the middle cerebral artery was gauged using transcranial Doppler ultrasonography. CA was evaluated by two methods: (1) transfer function analysis was calculated to determine the relationship between mean CBFV and mean arterial blood pressure (ABP) and (2) correlation index Mxa between mean CBFV and mean ABP.ONSD increased significantly during the first day, the third day and the first day of recovery of DI (P < 0.001).DI induced a reduction in Mxa index (P < 0.001) and an elevation in phase shift in low frequency bandwidth (P < 0.05). After DI, Mxa and coherence were strongly correlated with ONSD (P < 0.05) but not before DI. These results indicate that 3 days of DI induces significant changes in ONSD most likely reflecting an increase in ICP. CA was improved but also negatively correlated with ONSD suggesting that a persistent elevation ICP favors poor CA recovery after simulated microgravity.

It is well known that exposure to microgravity in astronauts leads to a plethora physiological responses such as headward fluid shift, body unloading, and cardiovascular deconditioning. When astronauts return to Earth, some encounter problems related to orthostatic intolerance. An impaired cerebral autoregulation (CA), which could be compromised by the effects of microgravity, has been proposed as one of the mechanisms responsible for orthostatic intolerance. CA is a homeostatic mechanism that maintains cerebral blood flow for any variations in cerebral perfusion pressure by adapting the vascular tone and cerebral vessel diameter. The groundbased models of microgravity are useful tools for determining the gravitational impact of spaceflight on human body. The head-down tilt bed rest (HDTBR), where the subject remains in supine position at −6 degrees for periods ranging from few days to several weeks is the most commonly used ground-based model of microgravity for cardiovascular deconditioning. head-down bed rest (HDBR) is able to replicate cephalic fluid shift, immobilization, confinement, and inactivity. Dry immersion (DI) model is another approach where the subject remains immersed in thermoneutral water covered with an elastic waterproof fabric separating the subject from the water. Regarding DI, this analog imitates absence of any supporting structure for the body, centralization of body fluids, immobilization and hypokinesia observed during spaceflight. However, little is known about the impact of microgravity on CA. Here, we review the fundamental principles and the different mechanisms involved in CA. We also consider the different approaches in order to assess CA. Finally, we focus on the effects of short-and long-term spaceflight on CA and compare these findings with two specific analogs to microgravity: HDBR and DI.

Aim Impairments in cerebral structure and cognitive performance in chronic heart failure (CHF) are critical components of its comorbidity spectrum. Autonomic afferents that arise from cardiac sensory fibres show enhanced activity with CHF. Desensitization of these fibres by local application of resiniferatoxin (RTX) during myocardial infarction (MI) is known to prevent cardiac hypertrophy, sympathetic hyperactivity and CHF. Whether these afferents mediate cerebral allostasis is unknown. Methods CHF was induced by myocardial infarction. To evaluate if cardiac afferents contribute to cerebral allostasis, RTX was acutely applied to the pericardial space in controls (RTX) and in MI treated animals (MI/RTX). Subjects were then evaluated in a series of behavioural tests recapitulating different symptoms of depressive disorders. Proteomics of the frontal cortices (FC) was performed to identify contributing proteins and pathways responsible for behavioural allostasis. Results Desensitization of cardiac afferents relieves hallmarks of an anxio/depressive‐like state in mice. Unique protein signatures and regulatory pathways in FCs isolated from each treatment reveal the degree of complexity inherent in the FC response to stresses originating in the heart. While cortices from the combined treatment (MI/RTX) did not retain protein signatures from the individual treatment groups, all three groups suffer dysregulation in circadian entrainment. Conclusion CHF is comorbid with an anxio/depressive‐like state and ablation of cardiac afferents relieves the despair phenotype. The strikingly different proteomic profiles observed in FCs suggest that MI and RTX lead to unique brain‐signalling patterns and that the combined treatment, potentially through destructive interference mechanisms, most closely resembles controls.