Abstract
Novel injectable biosensors were used to measure interstitial oxygenation before, during, and after transient ischemia. It is well known that reactive hyperemia occurs following a period of ischemia. However, increased blood flow does not necessarily mean increased oxygen tension in the tissue. Therefore, the purpose of this study was to test the hypothesis that tissue reactive hyperoxia occurs following release of hind-limb tourniquet occlusions. Rats were injected with bilateral hind-limb biosensors and were simultaneously subjected to a unilateral femoral vessel ligation. After approximately one and three months, the rats underwent a series of oxygenation challenges, including transient hind-limb tourniquet occlusion. Along with the biosensors, near infrared spectroscopy was used to measure percent oxyhemoglobin in capillaries and laser Doppler flowmetry was used to measure blood flow. Post-occlusion reactive hyperemia was observed. It was accompanied by tissue reactive hyperoxia, affirming that the post-occlusion oxygen supply must have exceeded the expected increased oxygen consumption. The measurement of the physiologic phenomenon of reactive hyperoxia could prove clinically beneficial for both diagnosis and optimizing therapy.
Highlights
One way to characterize such a response is by examining the behavior of blood flow upon release of an arterial occlusion
Throughout the duration of this study, all rats were in good health, with measurements and sensors well tolerated by the body
By combining data for healthy and ligated limbs and time points, we found the overall response magnitude for the peak independent of experimental group was significantly greater with phosphorescence biosensor than with near infrared (NIR) spectroscopy (p = 0.0065) (Fig. 7)
Summary
One way to characterize such a response is by examining the behavior of blood flow upon release of an arterial occlusion. During the period of occlusion, low perfusion pressure reduces vascular wall tension and leads to a local myogenic response causing vasodilation It tips the balance of vasoactive metabolites, such as adenosine, in favor of arteriolar vasodilation that decreases local microvascular resistance. Pain and hypothermia-mediated vasoconstriction, as well as vasoactive agents such as phenylephrine or norepinephrine can significantly influence extracranial blood contribution and subsequently alter NIR results[16] Other factors, such as differences in hemoglobin distribution between arterial, venous and capillary systems, false readings from myoglobin within the overlying fat and muscle, or interfering changes between the sensor and light source, such as occurs following tissue edema, can all influence NIR spectroscopy readings that may not necessarily reflect the true state of tissue oxygenation[17, 18]
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