From system to organ to cell: oxygenation and perfusion measurement in anesthesia and critical care

Schober, Patrick; Schwarte, Lothar A.

doi:10.1007/s10877-012-9350-4

Cited by 42 publications

(39 citation statements)

References 65 publications

(69 reference statements)

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“…In addition, high levels of oxygen (hyperoxia) are used in conjunction with anesthetics for protection against hypoxemia [1]. Further, hyperoxia is administered to premature newborn infants, which is believed to be a factor in the development of BPD [2].…”

Section: Introductionmentioning

confidence: 99%

Hyperoxia Decreases Glycolytic Capacity, Glycolytic Reserve and Oxidative Phosphorylation in MLE-12 Cells and Inhibits Complex I and II Function, but Not Complex IV in Isolated Mouse Lung Mitochondria

Das

2013

PLoS ONE

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High levels of oxygen (hyperoxia) are frequently used in critical care units and in conditions of respiratory insufficiencies in adults, as well as in infants. However, hyperoxia has been implicated in a number of pulmonary disorders including bronchopulmonary dysplasia (BPD) and adult respiratory distress syndrome (ARDS). Hyperoxia increases the generation of reactive oxygen species (ROS) in the mitochondria that could impair the function of the mitochondrial electron transport chain. We analyzed lung mitochondrial function in hyperoxia using the XF24 analyzer (extracellular flux) and optimized the assay for lung epithelial cells and mitochondria isolated from lungs of mice. Our data show that hyperoxia decreases basal oxygen consumption rate (OCR), spare respiratory capacity, maximal respiration and ATP turnover in MLE-12 cells. There was significant decrease in glycolytic capacity and glycolytic reserve in MLE-12 cells exposed to hyperoxia. Using mitochondria isolated from lungs of mice exposed to hyperoxia or normoxia we have shown that hyperoxia decreased the basal, state 3 and state3 μ (respiration in an uncoupled state) respirations. Further, using substrate or inhibitor of a specific complex we show that the OCR via complex I and II, but not complex IV was decreased, demonstrating that complexes I and II are specific targets of hyperoxia. Further, the activities of complex I (NADH dehydrogenase, NADH-DH) and complex II (succinate dehydrogenase, SDH) were decreased in hyperoxia, but the activity of complex IV (cytochrome oxidase, COX) remains unchanged. Taken together, our study show that hyperoxia impairs glycolytic and mitochondrial energy metabolism in in tact cells, as well as in lungs of mice by selectively inactivating components of electron transport system.

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Section: Introductionmentioning

confidence: 99%

Hyperoxia Decreases Glycolytic Capacity, Glycolytic Reserve and Oxidative Phosphorylation in MLE-12 Cells and Inhibits Complex I and II Function, but Not Complex IV in Isolated Mouse Lung Mitochondria

Das

2013

PLoS ONE

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“…Hyperoxia induced lung damage is of great clinical interest due to the use of oxygen therapy in the care and management of infants and adults with respiratory failure. Additionally, hyperoxia (30–100%) is frequently used in combination with volatile anesthetics such as sevoflurane for several hours in surgical procedures [1]. Animal studies have described the chronic and acute effects of elevated oxygen tension on the pulmonary alveolus [2–8].…”

Section: Introductionmentioning

confidence: 99%

Biphasic response of checkpoint control proteins in hyperoxia: exposure to lower levels of oxygen induces genome maintenance genes in experimental baboon BPD

Das

Wasnick

2014

Mol Cell Biochem

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Breathing high concentrations of oxygen (hyperoxia) causes lung injury and is associated with lung diseases such as bronchopulmonary dysplasia (BPD), respiratory distress syndrome (RDS) and persistent pulmonary hypertension of the newborns (PPHN). Hyperoxia (95–100%O2) causes DNA damage and growth arrest of lung cells and consequently cells die by apoptosis or necrosis. Although supplemental oxygen therapy is clinically important, the level and duration of hyperoxic exposure that would allow lung cells to reenter the cell cycle remains unclear. We hypothesized that cells exposed lower concentrations of hyperoxia will retain the capacity to enter cell cycle when recovered in room air. We employed varying concentrations of oxygen (21–95%) to determine the response of lung cells to hyperoxia. Our results indicate that cells were growth arrested and failed to reenter the cell cycle when exposed to greater than 60% oxygen. Cell cycle checkpoint proteins were increased in a biphasic manner, increasing until 70% oxygen, but declined in greater than 90% oxygen. Microarray analysis shows that there is significant decrease in the abundance of Cdks 6–8 and retinoblastoma protein (Rb), p107 and p130 in exposure to 90% oxygen for 48 hours. We further tested the effect of clinically relevant as needed oxygen [(pro-re-nada (prn)] in premature infant (125d and 140d) baboon model of bronchopulmonary dysplasia (BPD). The microarray results show that 6 or 14d PRN oxygen exposed animals had induced expression of chromosomal maintenance genes (MCMs), genes related to anti-inflammation, proliferation and differentiation.

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“…Characterization of tissue blood flow, blood oxygenation and oxidative metabolism is important for the diagnosis and therapeutic assessment of vascular/cellular diseases1234567. A wide range of imaging technologies have been developed to measure deep tissue hemodynamics/metabolism, including positron emission tomography (PET), magnetic resonance imaging (MRI), single photon emission computed tomography (SPECT), and Xenon computed tomography (Xenon CT).…”

mentioning

confidence: 99%

Simultaneous measurement of deep tissue blood flow and oxygenation using noncontact diffuse correlation spectroscopy flow-oximeter

Lin

Shang

et al. 2013

Sci Rep

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We report a novel noncontact diffuse correlation spectroscopy flow-oximeter for simultaneous quantification of relative changes in tissue blood flow (rBF) and oxygenation (Δ[oxygenation]). The noncontact probe was compared against a contact probe in tissue-like phantoms and forearm muscles (n = 10), and the dynamic trends in both rBF and Δ[oxygenation] were found to be highly correlated. However, the magnitudes of Δ[oxygenation] measured by the two probes were significantly different. Monte Carlo simulations and phantom experiments revealed that the arm curvature resulted in a significant underestimation (~−20%) for the noncontact measurements in Δ[oxygenation], but not in rBF. Other factors that may cause the residual discrepancies between the contact and noncontact measurements were discussed, and further comparisons with other established technologies are needed to identify/quantify these factors. Our research paves the way for noncontact and simultaneous monitoring of blood flow and oxygenation in soft and vulnerable tissues without distorting tissue hemodynamics.

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From system to organ to cell: oxygenation and perfusion measurement in anesthesia and critical care

Cited by 42 publications

References 65 publications

Hyperoxia Decreases Glycolytic Capacity, Glycolytic Reserve and Oxidative Phosphorylation in MLE-12 Cells and Inhibits Complex I and II Function, but Not Complex IV in Isolated Mouse Lung Mitochondria

Hyperoxia Decreases Glycolytic Capacity, Glycolytic Reserve and Oxidative Phosphorylation in MLE-12 Cells and Inhibits Complex I and II Function, but Not Complex IV in Isolated Mouse Lung Mitochondria

Biphasic response of checkpoint control proteins in hyperoxia: exposure to lower levels of oxygen induces genome maintenance genes in experimental baboon BPD

Simultaneous measurement of deep tissue blood flow and oxygenation using noncontact diffuse correlation spectroscopy flow-oximeter

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