Comprehensive Characterization of Cerebrovascular Dysfunction in Blast Traumatic Brain Injury Using Photoacoustic Microscopy

Rui Cao, Chenchu Zhang, Vladimir V. Mitkin, Miles F. Lankford, Jun Li, Zhiyi Zuo, Craig H. Meyer, Christopher P. Goyne, Stephen T. Ahlers, James R. Stone, Song Hu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


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 sO 2 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 sO 2 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.

Original languageEnglish
Pages (from-to)1526-1534
Number of pages9
JournalJournal of Neurotrauma
Issue number10
StatePublished - 15 May 2019
Externally publishedYes


  • blast traumatic brain injury
  • cerebrovascular reactivity
  • hemodynamics
  • oxygen metabolism
  • photoacoustic microscopy


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