Heterogeneity of Brain Oxidative Metabolism and Hypoxia Response

Dunn, Jeff F.; Rhodes, Eric S.; Panz, Tomasz

doi:10.1007/978-1-4615-5399-1_61

Cited by 8 publications

(4 citation statements)

References 27 publications

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“…Our baseline measurements of Pbr O 2 for anemic and control rats (17.3 Ϯ 4.1 and 19.5 Ϯ 3.7 Torr, respectively) were within the range reported for rat cerebral cortex (15.5 Ϯ 1.5 to 29.6 Ϯ 6 Torr) (7,8,39) and closer to the reported values for rat hippocampus (20 Ϯ 3 and 22 Ϯ 3 Torr) (8,31). These published values were achieved with the use of different invasive oxygen electrodes with diameters ranging from 50 to 300 m. They reflect the finding that measurements of cerebral tissue oxygen tension are ϳ10-15 Torr lower than corresponding sagittal sinus venous PO 2 values (7,28).…”

Section: Discussionsupporting

confidence: 83%

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Hemodilutional anemia is associated with increased cerebral neuronal nitric oxide synthase gene expression

Hare

Mazer

Mak

et al. 2003

Journal of Applied Physiology

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Severe hemodilutional anemia may reduce cerebral oxygen delivery, resulting in cerebral tissue hypoxia. Increased nitric oxide synthase (NOS) expression has been identified following cerebral hypoxia and may contribute to the compensatory increase in cerebral blood flow (CBF) observed after hypoxia and anemia. However, changes in cerebral NOS gene expression have not been reported after acute anemia. This study tests the hypothesis that acute hemodilutional anemia causes cerebral tissue hypoxia, triggering changes in cerebral NOS gene expression. Anesthetized rats underwent hemodilution when 30 ml/kg of blood were exchanged with pentastarch, resulting in a final hemoglobin concentration of 51.0 +/- 1.2 g/l (n = 7 rats). Caudate tissue oxygen tension (Pbr(O(2))) decreased transiently from 17.3 +/- 4.1 to 14.4 +/- 4.1 Torr (P < 0.05), before returning to baseline after approximately 20 min. An increase in CBF may have contributed to restoring Pbr(O(2)) by improving cerebral tissue oxygen delivery. An increase in neuronal NOS (nNOS) mRNA was detected by RT-PCR in the cerebral cortex of anemic rats after 3 h (P < 0.05, n = 5). A similar response was observed after exposure to hypoxia. By contrast, no increases in mRNA for endothelial NOS or interleukin-1beta were observed after anemia or hypoxia. Hemodilutional anemia caused an acute reduction in Pbr(O(2)) and an increase in cerebral cortical nNOS mRNA, supporting a role for nNOS in the physiological response to acute anemia.

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Section: Discussionsupporting

confidence: 83%

“…Data analysis. Pbr O 2 was normalized due to the known heterogeneity of cerebral tissue oxygenation levels between individual animals and within the brain (8). CBF measurements are presented as normalized data, recognizing that laser-Doppler flowmetry primarily reflects relative changes in red blood cell flux.…”

Section: Methodsmentioning

confidence: 99%

Hemodilutional anemia is associated with increased cerebral neuronal nitric oxide synthase gene expression

Hare

Mazer

Mak

et al. 2003

Journal of Applied Physiology

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“…Measurements of Pt O 2 with the use of polarographic microelectrodes have demonstrated significant variations between regions of the brain and within the cortex itself (14,25,29). This spatial heterogeneity may reflect differences in metabolic rate, perfusion rate, capillary density, and proportions of glial cells and neurons (14). Moreover, within a specific volume of brain cortex, Pt O 2 declines as a function of the radial distance from microvessels (46).…”

Section: Discussionmentioning

confidence: 99%

Critical oxygen tension in rat brain: a combined³¹P-NMR and EPR oximetry study

Rolett¹,

Azzawi

Liu

et al. 2000

American Journal of Physiology-Regulatory, Integrative and Comp

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The relationship between cerebral interstitial oxygen tension (Pt(O(2))) and cellular energetics was investigated in mechanically ventilated, anesthetized rats during progressive acute hypoxia to determine whether there is a "critical" brain Pt(O(2)) for maintaining steady-state aerobic metabolism. Cerebral Pt(O(2)), measured by electron paramagnetic resonance oximetry, decreased proportionately to inspired oxygen fraction. (31)P-nuclear magnetic resonance measurements revealed no changes in P(i), phosphocreatine (PCr)/P(i) ratio, or intracellular pH when arterial blood oxygen tension (Pa(O(2))) was reduced from 145.1 +/- 11.7 to 56.5 +/- 4.4 mmHg (means +/- SE). Intracellular acidosis, a sharp rise in P(i), and a decline in the PCr/P(i) ratio developed when Pa(O(2)) was reduced further to 40.7 +/- 2.3 mmHg. The corresponding Pt(O(2)) values were 15.1 +/- 1.8, 8.8 +/- 0.4, and 6.8 +/- 0.3 mmHg. We conclude that over a range of decreasing oxygen tensions, cerebral oxidative metabolism is not sensitive to oxygen concentration. Oxygen becomes a regulatory substrate, however, when Pt(O(2)) is decreased to a critical level.

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“…The unpaired mean values from the EPR measurements were significantly higher (P < 0.001) than Eppendorf means. If the comparison was limited to those values only down to 3.0 mm because of the expectation that the deeper data points might include regions of the brain that are expected to have lower PtO 2 (Dunn et al 1997), the values from the EPR measurements still were significantly higher than the Eppendorf means (P = 0.04).…”

Section: Rat Brain Pto 2 Assessed By Eppendorf Microelectrodesmentioning

confidence: 95%

Comparison of EPR oximetry and Eppendorf polarographic electrode assessments of rat brain PtO₂

et al. 2004

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EPR oximetry is a promising, relatively non-invasive method for monitoring the partial pressure of oxygen in tissue (PtO2) that has proved useful in following changes under various physiologic and pathophysiologic conditions. Optimal utilization of the method will be facilitated by systematic comparisons with other available methods. Here we report on the absolute values of rat brain PtO2 using EPR and the more widely used Eppendorf polarographic microelectrode system in the same brain. EPR used an L-band (1.2 GHz) spectrometer and implanted lithium phthalocyanine (LiPc) as the oxygen-sensitive paramagnetic material. Eppendorf measurements were made by a needle probe moved vertically through the cortex at 0.5 mm intervals in three tracks including one adjacent to the location of the LiPc. Several conclusions were drawn, including, (1) the average PtO2 measured by the two methods was similar but EPR reported a significantly higher average PtO2, (2) there was poor correlation between the values in the same animal on the same side of the brain, (3) the Eppendorf reported a larger range of values and (4) the heterogeneity of oxygen levels in the brain and the areas sampled by the two methods provide an adequate explanation for the observed differences.

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Heterogeneity of Brain Oxidative Metabolism and Hypoxia Response

Cited by 8 publications

References 27 publications

Hemodilutional anemia is associated with increased cerebral neuronal nitric oxide synthase gene expression

Hemodilutional anemia is associated with increased cerebral neuronal nitric oxide synthase gene expression

Critical oxygen tension in rat brain: a combined³¹P-NMR and EPR oximetry study

Comparison of EPR oximetry and Eppendorf polarographic electrode assessments of rat brain PtO₂

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Heterogeneity of Brain Oxidative Metabolism and Hypoxia Response

Cited by 8 publications

References 27 publications

Hemodilutional anemia is associated with increased cerebral neuronal nitric oxide synthase gene expression

Hemodilutional anemia is associated with increased cerebral neuronal nitric oxide synthase gene expression

Critical oxygen tension in rat brain: a combined31P-NMR and EPR oximetry study

Comparison of EPR oximetry and Eppendorf polarographic electrode assessments of rat brain PtO2

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Critical oxygen tension in rat brain: a combined³¹P-NMR and EPR oximetry study

Comparison of EPR oximetry and Eppendorf polarographic electrode assessments of rat brain PtO₂