ABSTRACT
The problem of capillary transport in fibrous porous materials at low levels of liquid saturation has been addressed. It has been demonstrated that the process of liquid spreading in this type of porous material at low saturation can be described macroscopically by a similar super-fast, nonlinear diffusion model to that which had been previously identified in experiments and simulations in particulate porous media. The macroscopic diffusion model has been underpinned by simulations using a microscopic network model. The theoretical results have been qualitatively compared with available experimental observations within the witness card technique using persistent liquids. The long-term evolution of the wetting spots was found to be truly universal and fully in line with the mathematical model developed. The result has important repercussions for the witness card technique used in field measurements of the dissemination of various low-volatility agents in imposing severe restrictions on collection and measurement times.
ABSTRACT
Blast traumatic brain injury (bTBI) is a leading contributor to combat-related injuries and death. Although substantial emphasis has been placed on blast-induced neuronal and axonal injuries, co-existing dysfunctions in the cerebral vasculature, particularly the microvasculature, remain poorly understood. Here, we studied blast-induced cerebrovascular dysfunctions in a rat model of bTBI (blast overpressure: 187.8 ± 18.3 kPa). Using photoacoustic microscopy (PAM), we quantified changes in cerebral hemodynamics and metabolism-including blood perfusion, oxygenation, flow, oxygen extraction fraction, and the metabolic rate of oxygen-4 h post-injury. Moreover, we assessed the effect of blast exposure on cerebrovascular reactivity (CVR) to vasodilatory stimulation. With vessel segmentation, we extracted these changes at the single-vessel level, revealing their dependence on vessel type (i.e., artery vs. vein) and diameter. We found that bTBI at this pressure level did not induce pronounced baseline changes in cerebrovascular diameter, blood perfusion, oxygenation, flow, oxygen extraction, and metabolism, except for a slight sO2 increase in small veins (<45 µm) and blood flow increase in large veins (≥45 µm). In contrast, this blast exposure almost abolished CVR, including arterial dilation, flow upregulation, and venous sO2 increase. This study is the most comprehensive assessment of cerebrovascular structure and physiology in response to blast exposure to date. The observed impairment in CVR can potentially cause cognitive decline due to the mismatch between cognitive metabolic demands and vessel's ability to dynamically respond to meet the demands. Also, the impaired CVR can lead to increased vulnerability of the brain to metabolic insults, including hypoxia and ischemia.
