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Hyperoxia-Induced ΔR 1

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Background and Purpose— Acceleration of longitudinal relaxation under hyperoxic challenge (ie, hyperoxia-induced ΔR 1 ) indicates oxygen accumulation and reflects baseline tissue oxygenation. We evaluated the feasibility of hyperoxia-induced ΔR 1 for evaluating cerebral oxygenation status and degree of ischemic damage in stroke. Methods— In 24-hour transient stroke rat models (n=13), hyperoxia-induced ΔR 1 , ischemic severity (apparent diffusion coefficient [ADC]), vasogenic edema (R 2 ), total and microvascular blood volume (superparamagnetic iron oxide-driven ΔR 2 * and ΔR 2 , respectively), and glucose metabolism activity ( 18 F-fluorodeoxyglucose uptake on positron emission tomography) were measured. The distribution of these parameters according to hyperoxia-induced ΔR 1 was analyzed. The partial pressure of tissue oxygen change during hyperoxic challenge was measured using fiberoptic tissue oximetry. In 4-hour stroke models (n=6), ADC and hyperoxia-induced ΔR 1 was analyzed with 2,3,5-triphenyltetrazolium chloride staining being a criterion of infarction. Results— Ischemic hemisphere showed significantly higher hyperoxia-induced ΔR 1 than nonischemic brain in a pattern depending on ADC. During hyperoxic challenge, ischemic hemisphere demonstrated uncontrolled increase of partial pressure of tissue oxygen, whereas contralateral hemisphere rapidly plateaued. Ischemic hemisphere also demonstrated significant correlation between hyperoxia-induced ΔR 1 and R 2 . Hyperoxia-induced ΔR 1 showed a significant negative correlation with 18 F-fluorodeoxyglucose uptake. The ADC, R 2 , ΔR 2 , and 18 F-fluorodeoxyglucose uptake showed a dichotomized distribution according to the hyperoxia-induced ΔR 1 as their slopes and values were higher at low hyperoxia-induced ΔR 1 (<50 ms −1 ) than at high ΔR 1 . In 4-hour stroke rats, the distribution of ADC according to the hyperoxia-induced ΔR 1 was similar with 24-hour stroke rats. The hyperoxia-induced ΔR 1 was greater in the infarct area (47±10 ms −1 ) than in peri-infarct area (16±4 ms −1 ; P <0.01). Conclusions— Hyperoxia-induced ΔR 1 adequately indicates cerebral oxygenation and can be a feasible biomarker to classify the degree of ischemia-induced damage in neurovascular function and metabolism in stroke brain.
Title: Hyperoxia-Induced ΔR 1
Description:
Background and Purpose— Acceleration of longitudinal relaxation under hyperoxic challenge (ie, hyperoxia-induced ΔR 1 ) indicates oxygen accumulation and reflects baseline tissue oxygenation.
We evaluated the feasibility of hyperoxia-induced ΔR 1 for evaluating cerebral oxygenation status and degree of ischemic damage in stroke.
Methods— In 24-hour transient stroke rat models (n=13), hyperoxia-induced ΔR 1 , ischemic severity (apparent diffusion coefficient [ADC]), vasogenic edema (R 2 ), total and microvascular blood volume (superparamagnetic iron oxide-driven ΔR 2 * and ΔR 2 , respectively), and glucose metabolism activity ( 18 F-fluorodeoxyglucose uptake on positron emission tomography) were measured.
The distribution of these parameters according to hyperoxia-induced ΔR 1 was analyzed.
The partial pressure of tissue oxygen change during hyperoxic challenge was measured using fiberoptic tissue oximetry.
In 4-hour stroke models (n=6), ADC and hyperoxia-induced ΔR 1 was analyzed with 2,3,5-triphenyltetrazolium chloride staining being a criterion of infarction.
Results— Ischemic hemisphere showed significantly higher hyperoxia-induced ΔR 1 than nonischemic brain in a pattern depending on ADC.
During hyperoxic challenge, ischemic hemisphere demonstrated uncontrolled increase of partial pressure of tissue oxygen, whereas contralateral hemisphere rapidly plateaued.
Ischemic hemisphere also demonstrated significant correlation between hyperoxia-induced ΔR 1 and R 2 .
Hyperoxia-induced ΔR 1 showed a significant negative correlation with 18 F-fluorodeoxyglucose uptake.
The ADC, R 2 , ΔR 2 , and 18 F-fluorodeoxyglucose uptake showed a dichotomized distribution according to the hyperoxia-induced ΔR 1 as their slopes and values were higher at low hyperoxia-induced ΔR 1 (<50 ms −1 ) than at high ΔR 1 .
In 4-hour stroke rats, the distribution of ADC according to the hyperoxia-induced ΔR 1 was similar with 24-hour stroke rats.
The hyperoxia-induced ΔR 1 was greater in the infarct area (47±10 ms −1 ) than in peri-infarct area (16±4 ms −1 ; P <0.
01).
Conclusions— Hyperoxia-induced ΔR 1 adequately indicates cerebral oxygenation and can be a feasible biomarker to classify the degree of ischemia-induced damage in neurovascular function and metabolism in stroke brain.

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