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Inner Retinal Oxygen Delivery and Metabolism in Streptozotocin Diabetic Rats
摘要： PURPOSE. The purpose of the study is to report global measurements of inner retinal oxygen delivery (DO2_IR) and oxygen metabolism (MO2_IR) in streptozotocin (STZ) diabetic rats. METHODS. Phosphorescence lifetime and blood flow imaging were performed in rats 4 (STZ/4wk; n = 10) and 6 (STZ/6wk; n = 10) weeks following injection of STZ to measure retinal arterial (O2A) and venous (O2V) oxygen contents and total retinal blood flow (F). DO2_IR and MO2_IR were calculated from measurements of F and O2A and of F and the arteriovenous oxygen content difference, respectively. Data in STZ rats were compared to those in healthy control rats (n = 10). RESULTS. Measurements of O2A and O2V were not significantly different among STZ/4wk, STZ/6wk, and control rats (P ≥ 0.28). Likewise, F was similar among all groups of rats (P = 0.81). DO2_IR measurements were 941 ± 231, 956 ± 232, and 973 ± 243 nL O2/min in control, STZ/4wk, and STZ/6wk rats, respectively (P = 0.95). MO2_IR measurements were 516 ± 175, 444 ± 103, and 496 ± 84 nL O2/min in control, STZ/4wk, and STZ/6wk rats, respectively (P = 0.37). CONCLUSIONS. Global inner retinal oxygen delivery and metabolism were not significantly impaired in STZ rats in early diabetes.
关键词： delivery,retina,rat,oxygen,metabolism,diabetes
更新于2025-09-23 15:22:29
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Comprehensive Characterization of Cerebrovascular Dysfunction in Blast Traumatic Brain Injury Using Photoacoustic Microscopy
摘要： 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, we quantified changes in cerebral hemodynamics and metabolism—including blood perfusion, oxygenation, flow, oxygen extraction fraction, and the metabolic rate of oxygen—4 hours post-injury. Moreover, we assessed the effect of blast exposure on cerebrovascular reactivity 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 sO2 increase in small veins (<45 μm) and blood flow increase in large veins (≥45 μm). In contrast, this blast exposure almost abolished cerebrovascular reactivity, including arterial dilation, flow upregulation, and venous sO2 increase. This study is the most comprehensive assessment of cerebrovascular structure and physiology in response to blast exposure to date. The observed impairment in cerebrovascular reactivity 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 cerebrovascular reactivity can lead to increased vulnerability of the brain to metabolic insults, including hypoxia and ischemia.
关键词： blast traumatic brain injury,cerebrovascular reactivity,photoacoustic microscopy,oxygen metabolism,hemodynamics
更新于2025-09-09 09:28:46