Microvascular oxygenation during simulated sleep apneaUsing Hyperspectral Imaging

Sleep-apnea includes brief, often cyclical interruptions in breathing rhythm (apneas) or temporary or sustained reductions in breath amplitude (hypopneas), which can cause significant arterial hypoxemia and hypercapnia. These events occur specifically during sleep and may involve: 1) a compromised or fully closed extrathoracic upper airway (“obstructive” event); 2) a significant reduction or cessation of brainstem respiratory motor output (“central” event); and 3) a combination of both central and obstructive events. Consequently, individuals experience recurrent cycles of intermittent hypoxia (IH), triggering physiological responses such as changes in cerebral oxygenation, endothelial dysfunction, platelet activation, and irregular cytokine profiles. Recent advancements in imaging techniques now allow for more detailed evaluation of IH’s effects on microcirculation and tissue adaptation to these cycles. To further evaluate the acute effects of IH, fully conscious Golden Syrian hamsters were instrumented with a dorsal skinfold window chamber and a catheter in the carotid artery. The animals were exposed to 30-second intervals cycling between 21% and 10% oxygen levels using a motorized switch this was done to simulate what we believe to be sleep apena. For proper controls, the same motorized switch was used to expose animals to cycling between 21% and 21% oxygen. In one set of experiments, oxygen saturation in the dorsal skinfold of a hamster was evaluated using a hyperspectral imaging system, capturing images every minute for the first 10 minutes and every 3 minutes for 60 minutes thereafter. In another set of experiments, microvascular hemodynamics (arterioles and venules) were measured in real-time at 30 minutes and 60 minutes. Across all experiments, parameters such as mean arterial pressure (MAP), heart rate (HR), full blood gases (pH, pCO 2 , pO 2 , SO 2 , and lactate), blood electrolyte composition (K + , Na + , Ca 2+ , and Cl − ), total hemoglobin concentration, and hematocrit were measured. We hypothesized that this approach would create a comprehensive profile of microvascular oxygenation in a simulated sleep apnea model. Our results confirmed that intermediate hypoxia was successfully induced, as the oxygen saturation in the experimental group dropped to 60%, and the MAP was significantly lower than in the control group. During the first 10 minutes, the experimental group recorded a drop in oxygen saturation in both arterioles and venules. This decrease was fitted to a one-phase decay model, yielding a rate constant of 0.398 min −1 in the venules and 1.014 min −1 in the arterioles. These results indicate a rapid decay in oxygen saturation during the initial phase, followed by stabilization with minimal variation. Micro-hemodynamic analysis revealed a significant drop in blood flow in arterioles and a substantial reduction in functional capillaries in the experimental group. This study demonstrates that the simulated sleep apnea model successfully induced intermediate hypoxia, characterized by rapid oxygen saturation decay and compromised microcirculation, followed by stabilization. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.