ArticleTranslational stroke research2026
A Ubiquitous Blood Flow Biomarker to Calculate Hypoxic-Ischemic Depolarization Latency in a Mouse Model of Focal Ischemic Stroke: Insight Into Metabolic and Electrophysiological Resilience.
Article in Translational stroke research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Focal cerebral ischemia, when sufficiently severe and prolonged, culminates in a near-complete loss of neuronal membrane potential in the ischemic core, known as hypoxic-ischemic depolarization (HID). The vasoconstrictive effect of HID causes an abrupt reduction in tissue blood flow. This cerebral blood flow signature marks the onset of HID and is easily detectable by conventional laser Doppler flowmetry or full-field optical imaging techniques. Using this blood flow signature in a model of endovascular filament occlusion of the middle cerebral artery (MCAO), we conducted a large retrospective study to investigate the latency between the onset of ischemia and HID. Leveraging aggregate laser Doppler flowmetry recordings (n = 289 mice) from several independent projects in our laboratory over a decade (2016-2025), we examined the robustness of HID latency as a biomarker, its biological and procedural predictors, and its ability to predict subsequent tissue outcome. We found that younger age (p = 0.008) and lower residual cerebral blood flow (p < 0.001) accelerate HID onset, while hypothermia (p = 0.029) and NMDA receptor blockade (p = 0.012) delay it. Furthermore, regression analysis shows that faster HID onset is associated with larger cortical, subcortical, and total infarct volumes (p = 0.005, 0.012, and 0.011, respectively) after MCAO. Altogether, our data suggest that HID latency, estimated from its hemodynamic signature in routine blood flow recordings during MCAO, can be a useful biomarker of metabolic and electrophysiological resilience in focal cerebral ischemia.
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