Noninvasive imaging of brain oxygen metabolism in children with primary nocturnal enuresis during natural sleep

Object Recent observations indicate that traumatic brain injury (TBI) may be associated with mitochondrial dysfunction. This, along with growing use of brain tissue PO2 monitors, has led to considerable interest in the potential use of ventilation with 100% oxygen to treat patients who have suffered a TBI. To date, the impact of normobaric hyperoxia has only been evaluated using indirect measures of its impact on brain metabolism. To determine if normobaric hyperoxia improves brain oxygen metabolism following acute TBI, the authors directly measured the cerebral metabolic rate for oxygen (CMRO2) with positron emission tomography before and after ventilation with 100% oxygen. Methods Baseline measurements of arterial and jugular venous blood gases, mean arterial blood pressure, intracranial pressure, cerebral blood flow (CBF), cerebral blood volume, oxygen extraction fraction, and CMRO2 were made at baseline while the patients underwent ventilation with a fraction of inspired oxygen (FiO2) of 0.3 to 0.5. The FiO2 was then increased to 1.0, and 1 hour later all measurements were repeated. Five patients were studied a mean of 17.9 ±5.8 hours (range 12–23 hours) after trauma. The median admission Glasgow Coma Scale score was 7 (range 3–9). During ventilation with 100% oxygen, there was a marked rise in PaO2 (from 117 ± 31 to 371 ± 99 mm Hg, p < 0.0001) and a small rise in arterial oxygen content (12.7 ± 4.0 to 13.3 ± 4.6 vol %, p = 0.03). There were no significant changes in systemic hemodynamic or other blood gas measurements. At the baseline evaluation, bihemispheric CBF was 39 ± 12 ml/100 g/min and bihemispheric CMRO2 was 1.9 ± 0.6 ml/100 g/min. During hyperoxia there was no significant change in either of these measurements. (Values are given as the mean ± standard deviation throughout.) Conclusions Normobaric hyperoxia did not improve brain oxygen metabolism. In the absence of outcome data from clinical trials, these preliminary data do not support the use of 100% oxygen in patients with acute TBI, although larger confirmatory studies are needed.

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Oxygen metabolism in acute ischemic stroke

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x17722095 ◽

2017 ◽

Vol 38 (9) ◽

pp. 1481-1499 ◽

Cited By ~ 8

Author(s):

Weili Lin ◽

William J Powers

Keyword(s):

Cerebral Ischemia ◽

Cerebral Metabolism ◽

Critical Factor ◽

Oxygen Metabolism ◽

Brain Oxygen ◽

Positron Emission ◽

Contrast Magnetic Resonance ◽

Wide Availability ◽

Magnetic Resonance Imaging Mri ◽

Brain Oxygen Metabolism

Gaining insights into brain oxygen metabolism has been one of the key areas of research in neurosciences. Extensive efforts have been devoted to developing approaches capable of providing measures of brain oxygen metabolism not only under normal physiological conditions but, more importantly, in various pathophysiological conditions such as cerebral ischemia. In particular, quantitative measures of cerebral metabolic rate of oxygen using positron emission tomography (PET) have been shown to be capable of discerning brain tissue viability during ischemic insults. However, the complex logistics associated with oxygen-15 PET have substantially hampered its wide clinical applicability. In contrast, magnetic resonance imaging (MRI)-based approaches have provided quantitative measures of cerebral oxygen metabolism similar to that obtained using PET. Given the wide availability, MRI-based approaches may have broader clinical impacts, particularly in cerebral ischemia, when time is a critical factor in deciding treatment selection. In this article, we review the pathophysiological basis of altered cerebral hemodynamics and oxygen metabolism in cerebral ischemia, how quantitative measures of cerebral metabolism were obtained using the Kety–Schmidt approach, the physical concepts of non-invasive oxygen metabolism imaging approaches, and, finally, clinical applications of the discussed imaging approaches.

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