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Chemical shift of 129 Xe dissolved in red blood cells: Application to a rat model of bronchopulmonary dysplasia
Author(s) -
Friedlander Yonni,
Zanette Brandon,
Lindenmaier Andras,
Sadanand Siddharth,
Li Daniel,
Stirrat Elaine,
Couch Marcus,
Kassner Andrea,
Jankov Robert P.,
Santyr Giles
Publication year - 2020
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.28121
Subject(s) - pulse oximetry , hyperoxia , cohort , oxygenation , bronchopulmonary dysplasia , oxygen saturation , fraction of inspired oxygen , hemoglobin , medicine , arterial blood , respiratory system , anesthesia , chemistry , gastroenterology , oxygen , lung , biology , mechanical ventilation , pregnancy , organic chemistry , genetics , gestational age
Purpose To measure the chemical shift of hyperpolarized 129 Xe dissolved in the red blood cells(δ RBC ) of a cohort of rats exposed to hyperoxia and intermittent hypoxia (IH) to mimic human bronchopulmonary dysplasia, and to investigate the effect of xenon‐blood distribution time on δ RBC . Methods δ RBC was measured from spectra acquired using a chemical shift saturation recovery sequence from 15 Sprague‐Dawley rats exposed to hyperoxia‐IH and 10 age‐matched control rats. Sensitization to the xenon‐blood distribution time was achieved by varying the time between saturation pulses, τ. δ RBC was compared with blood fraction measured by histology of the cohort and blood oxygenation measured directly using pulse oximetry following a hypoxic challenge in an identically exposed cohort. Results The mean δ RBC in the hyperoxia‐IH exposed rats was 0.55 ± 0.04 ppm lower than that of the healthy cohort ( P = .0038), and this difference did not depend on τ ( P = .996). The blood fraction of the exposed cohort was lower than that of the healthy cohort ( P = .0397). Oximetry measurements showed that the baseline arterial oxygen saturation (S a O 2 ) of each cohort was not different ( P = .72), but after a hypoxic challenge, the S a O 2 of the exposed cohort was lower than that of the healthy cohort ( P = .003). Conclusion δ RBC is reduced in rats exposed to hyperoxia‐IH compared with control rats. The change in δ RBC is consistent with enhanced blood oxygen desaturation of the exposed cohort measured by pulse oximetry during a hypoxic challenge. This suggests that the observed change in δ RBC reflects enhanced desaturation in the hyperoxia‐IH exposed cohort compared with the healthy cohort.