MRI Estimation of Global Brain Oxygen Consumption Rate

Jain, Varsha; Langham, Michael C; Wehrli, Félix W.

doi:10.1038/jcbfm.2011.20

Cited by 77 publications

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“…Measurements of CMRO 2 can help develop and guide treatment to ensure optimal oxygen utilization of the brain. Overall, baseline CMRO 2 in our cohort (Table 2) was 80% lower than typically observed in healthy adults, for whom values were reported in the range from 2 to 4 mL O 2 /minute per 100 g. 13,26,27 Literature on CMRO 2 in neonates is scarce, due in part to the limited number of modalities available for use in very young children. In a study using PET in critically ill neonates from the neonatal intensive care unit, Altman et al 28 noted CMRO 2 values of 0.06 to 0.54 mL O 2 / 100 g per minute in preterm infants and 0.4 to 1.3 mL O 2 /100 g per minute in sick term infants.…”

Section: Discussionmentioning

confidence: 54%

“…Unlike CMRO 2 , which is very rarely quantified in infants, the former parameters are cited in literature more often; however, the techniques used to quantify these parameters are typically invasive, employing arterial or venous blood draws or the use of radioactive tracers. We observed a median resting-state CBF of 9.58 mL/minute per 100 gB20% of normal adult CBF, which is typically around 50 mL/minute per 100 g, 13,26,27 and B30% to 50% of healthy neonatal CBF in the frontal cortex, which Chiron et al reported as 34±3.5 mL/minute per 100 g (using SPECT with 133 Xe) and Miranda et al reported as 16.6 ± 5.9 mL/minute per 100 g (using arterial spin labeled perfusion MRI, ASL pMRI). 29,30 Licht et al 7 measured CBF with ASL perfusion MRI in a similar population of 25 term infants with CHD, found average resting CBF of 19.73 ± 9.15 mL/minute per 100 g, or approximately twice our current reported values.…”

Section: Discussionmentioning

confidence: 65%

“…Specifically, S v O 2 was quantified using MRI susceptometry-based oximetry and CBF via PC MRI. Details on the pulse sequence are in Jain et al 13,20 The scan parameters were as follows: voxel size Anatomic T 1 -and T 2 -weighted high-resolution MRI was performed and neonatal brain volumes were estimated from the resulting images using standard segmentation techniques to obtain CBF and CMRO 2 in conventional units of mL/minute per 100 g and mL O 2 /100 g per minute, respectively.…”

Section: Magnetic Resonance Imaging Measurementsmentioning

confidence: 99%

“…8 However, while quantification of total brain blood flow is relatively straightforward, measurement of cerebral venous oxygen saturation (S v O 2 ), the other key component required to quantify CMRO 2 , is not. Two different approaches have emerged to address the quantification of S v O 2 , both making use of the venous blood's paramagnetism: (1) Transverse relaxationbased methods (for example, T 2 Relaxation Under Spin Tagging TRUST, 9 and Quantitative Imaging of Extraction of Oxygen and Tissue Consumption, QUIXOTIC 10 ), and (2) susceptometric techniques that quantify the blood's magnetic susceptibility, which is linearly related to deoxyhemoglobin concentration [11][12][13] (for example phase-based measurement of regional oxygen concentration, PROM 14 ).…”

Section: Introductionmentioning

confidence: 99%

“…The MRI method measures venous blood oxygen saturation in the superior sagittal sinus (SSS) via MRI susceptometry [11][12][13] and, simultaneously, CBF by PC MRI; the combination yields global CMRO 2 in absolute physiologic units. The optical method utilizes a portable bedside instrument to probe regional microvascular tissue oxygenation, perfusion, and metabolism in the frontal cortex.…”

Section: Introductionmentioning

confidence: 99%

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Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics

Jain

Buckley

Licht

et al. 2013

J Cereb Blood Flow Metab

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158

179

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Neonatal congenital heart disease (CHD) is associated with altered cerebral hemodynamics and increased risk of brain injury. Two novel noninvasive techniques, magnetic resonance imaging (MRI) and diffuse optical and correlation spectroscopies (diffuse optical spectroscopy (DOS), diffuse correlation spectroscopy (DCS)), were employed to quantify cerebral blood flow (CBF) and oxygen metabolism (CMRO 2 ) of 32 anesthetized CHD neonates at rest and during hypercapnia. Cerebral venous oxygen saturation (S v O 2 ) and CBF were measured simultaneously with MRI in the superior sagittal sinus, yielding global oxygen extraction fraction (OEF) and global CMRO 2 in physiologic units. In addition, microvascular tissue oxygenation (StO 2 ) and indices of microvascular CBF (BFI) and CMRO 2 (CMRO 2i ) in the frontal cortex were determined by DOS/DCS. Median resting-state MRI-measured OEF, CBF, and CMRO 2 were 0.38, 9.7 mL/minute per 100 g and 0.52 mL O 2 /minute per 100 g, respectively. These CBF and CMRO 2 values are lower than literature reports for healthy term neonates (which are sparse and quantified using different methods) and resemble values reported for premature infants. Keywords: cerebral blood flow; cerebral hemodynamics; diffuse optics; MRI; near-infrared spectroscopy; neonatal ischemia INTRODUCTION Congenital heart disease (CHD) affects B35,000 neonates each year in the United States. These patients suffer both short-and long-term neurologic sequelae. Periventricular leukomalacia is the most common cerebral injury found in this population. This type of injury is characterized by focal necrosis in the periventricular white matter, and it is associated with pyknotic glial nuclei and reactive gliosis. 1,2 During the early stages of brain development, the oligodendrocyte (brain glial cells) precursors are metabolically very active and highly susceptible to injury from reduced blood flow and oxygen delivery. Hence, hypoxiaischemia has been implicated as a major cause of this injury in CHD neonates.Periventricular leukomalacia leads to impaired myelination and has been linked to worse neurodevelopmental outcomes in premature infants and postulated to cause (at least in part) the impaired cognition and cerebral palsy commonly seen in this cohort of infants with CHD. 3,4 Quantification of the hemodynamic and metabolic state of these neonates via measurements of cerebral blood flow (CBF) and the cerebral metabolic rate of oxygen consumption (CMRO 2 ) should provide valuable information toward understanding the interaction between cardiac pathophysiology and subsequent cerebral health. Potentially, such new knowledge could help predict and prevent adverse outcomes.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 65%

Section: Magnetic Resonance Imaging Measurementsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics

Jain

Buckley

Licht

et al. 2013

J Cereb Blood Flow Metab

Self Cite

158

179

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Investigation of BOLD fMRI resonance frequency shifts and quantitative susceptibility changes at 7 T

Bianciardi

Gelderen

Duyn

2013

Human Brain Mapping

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Although blood oxygenation level dependent (BOLD) functional magnetic resonance imaging (fMRI) experiments of brain activity generally rely on the magnitude of the signal, they also provide frequency information that can be derived from the phase of the signal. However, because of confounding effects of instrumental and physiological origin, BOLD related frequency information is difficult to extract and therefore rarely used. Here, we explored the use of high field (7 T) and dedicated signal processing methods to extract frequency information and use it to quantify and interpret blood oxygenation and blood volume changes. We found that optimized preprocessing improves detection of task-evoked and spontaneous changes in phase signals and resonance frequency shifts over large areas of the cortex with sensitivity comparable to that of magnitude signals. Moreover, our results suggest the feasibility of mapping BOLD quantitative susceptibility changes in at least part of the activated area and its largest draining veins. Comparison with magnitude data suggests that the observed susceptibility changes originate from neuronal activity through induced blood volume and oxygenation changes in pial and intracortical veins. Further, from frequency shifts and susceptibility values, we estimated that, relative to baseline, the fractional oxygen saturation in large vessels increased by 0.02–0.05 during stimulation, which is consistent to previously published estimates. Together, these findings demonstrate that valuable information can be derived from fMRI imaging of BOLD frequency shifts and quantitative susceptibility changes.

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The role of the red blood cell and platelet in the evolution of mammalian and avian endothermy

Soslau

2019

J Exp Zool Pt B

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This review presents evidence to support the hypothesis that the reduced O2 during the Permian/Triassic period was the impetus for the evolutionary selection of endothermic animals. The evolution of smaller red blood cells with greater surface areas along with increased: capillary density, capillary surface area, hematocrits, blood pressure, blood flow rates, and shear rates were critical for efficient gas exchange in endothermy. The evolution of the four‐chambered mammalian/avian heart allowed for low pulmonary and high systemic blood pressure. It is proposed that hypoxia‐induced angiogenesis led to increased vascularization in endothermic animals. The increased blood pressure, flow rates, and shear forces likely required changes in hemostatic mechanisms that were met in mammals by the evolution of anucleate platelets. The evolution of mammals and birds occurred in a parallel fashion with further genetic changes to anucleate RBCs/platelets occurring in mammals. Although it is possible that the evolution of endothermy in birds and mammals occurred as two independent events, it is more likely that a common ancestor developed genetic mutations that laid down the road map for parallel alterations of their cardiovascular system in response to environmental pressures. Model systems to support the proposed changes from ectotherm to endotherm were developed from published data. The evolutionary development of endothermy occurred over millions of years with a continuum of genetic alterations that involved skeletal, soft tissue, cardiovascular macrochanges along with numerous molecular alterations. Genetic signals and potential regulators for the evolutionary changes of endothermic blood cells from their bipotential stem cells are also proposed.

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MRI Estimation of Global Brain Oxygen Consumption Rate

Abstract: Following the publication of this article, the author's noted a misprint in equation (4). The equation should read: %HbO 2 ¼ 1 À 2jDfj gDw do B o DTEðcos 2 y À 1=3ÞHct Â100

Cited by 77 publications

References 0 publications

Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics

Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics

Investigation of BOLD fMRI resonance frequency shifts and quantitative susceptibility changes at 7 T

The role of the red blood cell and platelet in the evolution of mammalian and avian endothermy

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