Abstract
The optical attenuation coefficient (OAC) estimated using optical coherence tomography (OAC-OCT) offers a label-free 3D mapping of tissue infarction, but the physiological origin of the OAC contrast remains unclear. For effectively suppressing OAC fluctuations, we propose a hybrid (wavelength/angle) division multiplexing (HDM) method, which improved the OAC contrast by 70.7% in tissue phantoms. To test the feasibility of OAC-based infarction detection, triphenyltetrazolium chloride (TTC) staining was performed on fresh ex vivo brain slices, and the TTC-defined infarction was used as the ground truth. Sharp OAC contrast was observed between the TTC-defined infarction (1.09 mm-1) and normal tissue (0.79 mm-1). The OAC infarction spatially matched well with the TTC-defined infarction. To further explore the physiological origin of OAC contrast in ischemic stroke at the cellular level, the dynamic changes in OAC were measured in the rat cortex in vivo over 3 weeks after photothrombosis (PT) occlusion and found significantly correlated with the changes in astrocytes and neurons acquired with ex vivo hematoxylin and eosin (HE), glial fibrillary acidic protein (GFAP), and NeuN staining. These results suggest that OAC imaging enables non-invasive infarction detection and its contrast might originate from the changes in astrocytes and neurons in the chronic PT stroke model. The cellular responses revealed by in vivo OAC imaging would be essential for evaluating treatments and even developing novel therapies.