Abstract
Visible-light optical coherence tomography (Vis-OCT) is an emerging technology that can image hemodynamic response in microvasculature. Vis-OCT can retrieve blood oxygen saturation (sO2) mapping using intrinsic optical absorption contrast while providing high-resolution anatomical vascular structures at the same time. To improve the accuracy of Vis-OCT oximetry on vessels embedded in highly scattering medium, i.e., brain cortex, we developed and formulated a novel dual-depth sampling and normalization strategy that allowed us to minimize the detrimental effect of ubiquitous tissue scattering. We applied our newly developed approach to monitor the hemodynamic response in mouse cortex after focal photothrombosis. We observed vessel dilatation, which was negatively correlated with the original vessel diameter, in the penumbra region. The sO2 of vessels in the penumbra region also dropped below normal range after focal ischemia.
Highlights
Continuous cerebral circulation and sufficient oxygen supply are critical for maintaining the normal functionality of the brain [1]
The ischemic core can be identified, as the optical coherence tomography (OCT) angiography intensity within the region fell below our detection sensitivity due to the lack of flow-enhanced motion contrast [Fig. 3(b)]
We believe the slight shift was caused by a certain degree of edema and fluid accumulation that developed after vessel occlusion [25]
Summary
Continuous cerebral circulation and sufficient oxygen supply are critical for maintaining the normal functionality of the brain [1]. During ischemic stroke (IS), impairments of the vascular network restrict the ability of brain to regulate blood supply [2]. Reduced cerebral blood flow (CBF) results in a shortage of oxygen delivery and the accumulation of toxic metabolic wastes, causing irreversible brain injury [3]. In the ischemic core, where the blood supply relies solely on the occluded vessel, excitotoxicity and acidotoxicity contribute to acute neuron necrosis. In the penumbra region, where collateral blood flow can maintain certain cell functions, delayed neuron death may be caused by peri-infarct depolarization, oxidative and nitrative stress, inflammation, and apoptosis [3,4,5]
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