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Hyperoxia-Induced ΔR1.

Ji-Yeon Suh1,2, Gyunggoo Cho2, Youngkyu Song2

  • 1From the Department of Radiology, Research Institute of Radiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea (J.-Y.S., D.-C.W., B.W.P., W.H.S., J.K.K.).

Stroke
|December 21, 2018
PubMed
Summary

Hyperoxia-induced ΔR1 effectively measures cerebral oxygenation and stroke-induced damage. This biomarker correlates with ischemia severity, reflecting neurovascular function and metabolism in stroke patients.

Keywords:
brain infarctionhyperoxiamagnetic resonance imagingtissue metabolism

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Area of Science:

  • Neuroimaging
  • Biomarkers
  • Stroke Research

Background:

  • Hyperoxia-induced ΔR1 quantifies oxygen accumulation, reflecting tissue oxygenation.
  • Assessing cerebral oxygenation and ischemic damage in stroke is crucial for effective treatment.

Purpose of the Study:

  • To evaluate the feasibility of hyperoxia-induced ΔR1 for assessing cerebral oxygenation.
  • To determine its utility in quantifying ischemic damage and its impact on neurovascular function and metabolism in stroke models.

Main Methods:

  • Utilized transient stroke rat models (24-hour and 4-hour) to measure hyperoxia-induced ΔR1.
  • Correlated hyperoxia-induced ΔR1 with apparent diffusion coefficient (ADC), vasogenic edema (R2), blood volume changes (ΔR2*, ΔR2), and glucose metabolism (18F-fluorodeoxyglucose PET).
  • Measured tissue oxygen partial pressure changes during hyperoxic challenge using fiberoptic oximetry.

Main Results:

  • Ischemic hemispheres exhibited significantly higher hyperoxia-induced ΔR1 compared to non-ischemic hemispheres, correlating with ADC.
  • A significant correlation was observed between hyperoxia-induced ΔR1 and vasogenic edema (R2).
  • Hyperoxia-induced ΔR1 showed a negative correlation with glucose metabolism and was higher in infarct areas.

Conclusions:

  • Hyperoxia-induced ΔR1 is a feasible biomarker for assessing cerebral oxygenation status in stroke.
  • It effectively classifies the degree of ischemia-induced damage, reflecting alterations in neurovascular function and metabolism.