scholarly journals Carbogen-induced increases in tumor oxygenation depend on the vascular status of the tumor: A multiparametric MRI study in two rat glioblastoma models

2016 ◽  
Vol 37 (6) ◽  
pp. 2270-2282 ◽  
Author(s):  
Ararat Chakhoyan ◽  
Aurélien Corroyer-Dulmont ◽  
Marine M Leblond ◽  
Aurélie Gérault ◽  
Jérôme Toutain ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Blood Oxygenation Level Dependent ◽  
Blood Oxygenation ◽  
Blood Oxygen ◽  
Blood Oxygen Saturation ◽  
Blood Oxygenation Level ◽  
Oxygenation Level ◽  
Volume Blood

The alleviation of hypoxia in glioblastoma with carbogen to improve treatment has met with limited success. Our hypothesis is that the eventual benefits of carbogen depend on the capacity for vasodilation. We examined, with MRI, changes in fractional cerebral blood volume, blood oxygen saturation, and blood oxygenation level dependent signals in response to carbogen. The analyses were performed in two xenograft models of glioma (U87 and U251) recognized to have different vascular patterns. Carbogen increased fractional cerebral blood volume, blood oxygen saturation, and blood oxygenation level dependent signals in contralateral tissues. In the tumor core and peritumoral regions, changes were dependent on the capacity to vasodilate rather than on resting fractional cerebral blood volume. In the highly vascularised U87 tumor, carbogen induced a greater increase in fractional cerebral blood volume and blood oxygen saturation in comparison to the less vascularized U251 tumor. The blood oxygenation level dependent signal revealed a delayed response in U251 tumors relative to the contralateral tissue. Additionally, we highlight the considerable heterogeneity of fractional cerebral blood volume, blood oxygen saturation, and blood oxygenation level dependent within U251 tumor in which multiple compartments co-exist (tumor core, rim and peritumoral regions). Finally, our study underlines the complexity of the flow/metabolism interactions in different models of glioblastoma. These irregularities should be taken into account in order to palliate intratumoral hypoxia in clinical trials.

Evaluation of a quantitative blood oxygenation level-dependent (qBOLD) approach to map local blood oxygen saturation

2010 ◽  
pp. n/a-n/a ◽  
Author(s):  
Thomas Christen ◽  
Benjamin Lemasson ◽  
Nicolas Pannetier ◽  
Régine Farion ◽  
Christoph Segebarth ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
Blood Oxygenation Level Dependent ◽  
Blood Oxygenation ◽  
Blood Oxygen ◽  
Blood Oxygen Saturation ◽  
Blood Oxygenation Level ◽  
Oxygenation Level

scholarly journals Simultaneous Blood Oxygenation Level-Dependent and Cerebral Blood Flow Functional Magnetic Resonance Imaging during Forepaw Stimulation in the Rat

1999 ◽  
Vol 19 (8) ◽  
pp. 871-879 ◽  
Author(s):  
Afonso C. Silva ◽  
Sang-Pil Lee ◽  
Guang Yang ◽  
Costantino Iadecola ◽  
Seong-Gi Kim
Keyword(s):  
Correlation Coefficient ◽  
Cerebral Blood Volume ◽  
Blood Oxygenation Level Dependent ◽  
Blood Oxygenation ◽  
Single Shot ◽  
Bold Signal ◽  
Doppler Flowmetry ◽  
Blood Oxygenation Level ◽  
Oxygenation Level ◽  
Signal Changes

The blood oxygenation level-dependent (BOLD) contrast mechanism can be modeled as a complex interplay between CBF, cerebral blood volume (CBV), and CMRO2. Positive BOLD signal changes are presumably caused by CBF changes in excess of increases in CMRO2. Because this uncoupling between CBF and CMRO2 may not always be present, the magnitude of BOLD changes may not be a good index of CBF changes. In this study, the relation between BOLD and CBF was investigated further. Continuous arterial spin labeling was combined with a single-shot, multislice echo-planar imaging to enable simultaneous measurements of BOLD and CBF changes in a well-established model of functional brain activation, the electrical forepaw stimulation of a-chloralose-anesthetized rats. The paradigm consisted of two 18- to 30-second stimulation periods separated by a 1-minute resting interval. Stimulation parameters were optimized by laser Doppler flowmetry. For the same cross-correlation threshold, the BOLD and CBF active maps were centered within the size of one pixel (470 µm). However, the BOLD map was significantly larger than the CBF map. Measurements taken from 15 rats at 9.4 T using a 10-millisecond echo-time showed 3.7 ± 1.7% BOLD and 125.67 ± 81.7% CBF increases in the contralateral somatosensory cortex during the first stimulation, and 2.6 ± 1.2% BOLD and 79.3 ± 43.6% CBF increases during the second stimulation. The correlation coefficient between BOLD and CBF changes was 0.89. The overall temporal correlation coefficient between BOLD and CBF time-courses was 0.97. These results show that under the experimental conditions of the current study, the BOLD signal changes follow the changes in CBF.

scholarly journals Quantitative analysis of the postcontractile blood-oxygenation-level-dependent (BOLD) effect in skeletal muscle

2011 ◽  
Vol 111 (1) ◽  
pp. 27-39 ◽  
Author(s):  
Theodore F. Towse ◽  
Jill M. Slade ◽  
Jeffrey A. Ambrose ◽  
Mark C. DeLano ◽  
Ronald A. Meyer
Keyword(s):  
Blood Volume ◽  
Near Infrared ◽  
Blood Oxygenation Level Dependent ◽  
Blood Oxygenation ◽  
Activity Level ◽  
Anterior Tibial Artery ◽  
Physically Active ◽  
Hemoglobin Saturation ◽  
Blood Oxygenation Level ◽  
Oxygenation Level

Previous studies show that transient increases in both blood flow and magnetic resonance image signal intensity (SI) occur in human muscle after brief, single contractions, and that the SI increases are threefold larger in physically active compared with sedentary subjects. This study examined the relationship between these transient changes by measuring anterior tibial artery flow (Doppler ultrasound), anterior muscle SI (3T, one-shot echo-planar images, TR/TE = 1,000/35), and muscle blood volume and hemoglobin saturation [near-infrared spectroscopy (NIRS)] in the same subjects after 1-s-duration maximum isometric ankle dorsiflexion contractions. Arterial flow increased to a peak 5.9 ± 0.7-fold above rest (SE, n = 11, range 2.6–10.2) within 7 s and muscle SI increased to a peak 2.7 ± 0.6% (range 0.0–6.0%) above rest within 12 s after the contractions. The peak postcontractile SI change was significantly correlated with both peak postcontractile flow ( r = 0.61, n = 11) and with subject activity level ( r = 0.63, n = 10) estimated from 7-day accelerometer recordings. In a subset of 7 subjects in which NIRS data acquisition was successful, the peak magnitude of the postcontractile SI change agreed well with SI calculated from the NIRS blood volume and saturation changes ( r = 0.80, slope = 1.02, intercept = 0.16), confirming the blood-oxygenation-level-dependent (BOLD) mechanism underlying the SI change. The magnitudes of postcontractile changes in blood saturation and SI were reproduced by a simple one-compartment muscle vascular model that incorporated the observed pattern of postcontractile flow, and which assumed muscle O2 consumption peaks within 2 s after a brief contraction. The results show that muscle postcontractile BOLD SI changes depend critically on the balance between O2 delivery and O2 consumption, both of which can be altered by chronic physical activity.

scholarly journals Biophysical and Physiological Origins of Blood Oxygenation Level-Dependent fMRI Signals

2012 ◽  
Vol 32 (7) ◽  
pp. 1188-1206 ◽  
Author(s):  
Seong-Gi Kim ◽  
Seiji Ogawa
Keyword(s):  
Cerebral Blood Volume ◽  
Volume Fraction ◽  
Spin Echo ◽  
Blood Oxygenation Level Dependent ◽  
Blood Oxygenation ◽  
Dynamic Responses ◽  
Bold Fmri ◽  
Functional Changes ◽  
Blood Oxygenation Level ◽  
Oxygenation Level

After its discovery in 1990, blood oxygenation level-dependent (BOLD) contrast in functional magnetic resonance imaging (fMRI) has been widely used to map brain activation in humans and animals. Since fMRI relies on signal changes induced by neural activity, its signal source can be complex and is also dependent on imaging parameters and techniques. In this review, we identify and describe the origins of BOLD fMRI signals, including the topics of (1) effects of spin density, volume fraction, inflow, perfusion, and susceptibility as potential contributors to BOLD fMRI, (2) intravascular and extravascular contributions to conventional gradient-echo and spin-echo BOLD fMRI, (3) spatial specificity of hemodynamic-based fMRI related to vascular architecture and intrinsic hemodynamic responses, (4) BOLD signal contributions from functional changes in cerebral blood flow (CBF), cerebral blood volume (CBV), and cerebral metabolic rate of O2 utilization (CMRO2), (5) dynamic responses of BOLD, CBF, CMRO2, and arterial and venous CBV, (6) potential sources of initial BOLD dips, poststimulus BOLD undershoots, and prolonged negative BOLD fMRI signals, (7) dependence of stimulus-evoked BOLD signals on baseline physiology, and (8) basis of resting-state BOLD fluctuations. These discussions are highly relevant to interpreting BOLD fMRI signals as physiological means.

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