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A model of brain circulation and metabolism: NIRS signal changes during physiological challenges.

Banaji M, Mallet A, Elwell CE, Nicholls P, Cooper CE - PLoS Comput. Biol. (2008)

Bottom Line: We anticipate that the model will play an important role in helping to understand the NIRS signals, in particular, the cytochrome signal, which has been hard to interpret.A range of model simulations are presented, and model outputs are compared to published data obtained from both in vivo and in vitro settings.The comparisons are encouraging, showing that the model is able to reproduce observed behaviour in response to various stimuli.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, University of Essex, Colchester, United Kingdom. m.banaji@ucl.ac.uk

ABSTRACT
We construct a model of brain circulation and energy metabolism. The model is designed to explain experimental data and predict the response of the circulation and metabolism to a variety of stimuli, in particular, changes in arterial blood pressure, CO(2) levels, O(2) levels, and functional activation. Significant model outputs are predictions about blood flow, metabolic rate, and quantities measurable noninvasively using near-infrared spectroscopy (NIRS), including cerebral blood volume and oxygenation and the redox state of the Cu(A) centre in cytochrome c oxidase. These quantities are now frequently measured in clinical settings; however the relationship between the measurements and the underlying physiological events is in general complex. We anticipate that the model will play an important role in helping to understand the NIRS signals, in particular, the cytochrome signal, which has been hard to interpret. A range of model simulations are presented, and model outputs are compared to published data obtained from both in vivo and in vitro settings. The comparisons are encouraging, showing that the model is able to reproduce observed behaviour in response to various stimuli.

Show MeSH
Relationship between CMRO2 and mitochondrial oxygen levels                            during activation.The full model was run with parameter Ru set                            to zero so that an increase in demand had no effect on blood flow.                            Increasing u allowed increases in CMRO2 up                            to approximately 145 percent of baseline. The three data points shown                            are calculated from Figure                                2 of [55] in which predictions on how tissue                            oxygen levels in the “lethal corner” should vary                            with activation level during normoxia are presented.
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pcbi-1000212-g008: Relationship between CMRO2 and mitochondrial oxygen levels during activation.The full model was run with parameter Ru set to zero so that an increase in demand had no effect on blood flow. Increasing u allowed increases in CMRO2 up to approximately 145 percent of baseline. The three data points shown are calculated from Figure 2 of [55] in which predictions on how tissue oxygen levels in the “lethal corner” should vary with activation level during normoxia are presented.

Mentions: It is also interesting to note this work supports the conclusion of [55]: That in the physiological range, an increase in CBF is not required for the observed increase in CMRO2 to take place. In order to verify this, the full model was run with Ru = 0 so that demand had no effect on blood flow. Again, significant increases in CMRO2 – up to about 45 percent – could occur. The relationship between oxygen levels and CMRO2 was also consistent with data in [55] as shown in Figure 8.


A model of brain circulation and metabolism: NIRS signal changes during physiological challenges.

Banaji M, Mallet A, Elwell CE, Nicholls P, Cooper CE - PLoS Comput. Biol. (2008)

Relationship between CMRO2 and mitochondrial oxygen levels                            during activation.The full model was run with parameter Ru set                            to zero so that an increase in demand had no effect on blood flow.                            Increasing u allowed increases in CMRO2 up                            to approximately 145 percent of baseline. The three data points shown                            are calculated from Figure                                2 of [55] in which predictions on how tissue                            oxygen levels in the “lethal corner” should vary                            with activation level during normoxia are presented.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2573000&req=5

pcbi-1000212-g008: Relationship between CMRO2 and mitochondrial oxygen levels during activation.The full model was run with parameter Ru set to zero so that an increase in demand had no effect on blood flow. Increasing u allowed increases in CMRO2 up to approximately 145 percent of baseline. The three data points shown are calculated from Figure 2 of [55] in which predictions on how tissue oxygen levels in the “lethal corner” should vary with activation level during normoxia are presented.
Mentions: It is also interesting to note this work supports the conclusion of [55]: That in the physiological range, an increase in CBF is not required for the observed increase in CMRO2 to take place. In order to verify this, the full model was run with Ru = 0 so that demand had no effect on blood flow. Again, significant increases in CMRO2 – up to about 45 percent – could occur. The relationship between oxygen levels and CMRO2 was also consistent with data in [55] as shown in Figure 8.

Bottom Line: We anticipate that the model will play an important role in helping to understand the NIRS signals, in particular, the cytochrome signal, which has been hard to interpret.A range of model simulations are presented, and model outputs are compared to published data obtained from both in vivo and in vitro settings.The comparisons are encouraging, showing that the model is able to reproduce observed behaviour in response to various stimuli.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, University of Essex, Colchester, United Kingdom. m.banaji@ucl.ac.uk

ABSTRACT
We construct a model of brain circulation and energy metabolism. The model is designed to explain experimental data and predict the response of the circulation and metabolism to a variety of stimuli, in particular, changes in arterial blood pressure, CO(2) levels, O(2) levels, and functional activation. Significant model outputs are predictions about blood flow, metabolic rate, and quantities measurable noninvasively using near-infrared spectroscopy (NIRS), including cerebral blood volume and oxygenation and the redox state of the Cu(A) centre in cytochrome c oxidase. These quantities are now frequently measured in clinical settings; however the relationship between the measurements and the underlying physiological events is in general complex. We anticipate that the model will play an important role in helping to understand the NIRS signals, in particular, the cytochrome signal, which has been hard to interpret. A range of model simulations are presented, and model outputs are compared to published data obtained from both in vivo and in vitro settings. The comparisons are encouraging, showing that the model is able to reproduce observed behaviour in response to various stimuli.

Show MeSH