Regional Gas Exchange and Cellular Metabolic Activity in Ventilator-induced Lung Injury

Musch, Guido; Venegas, José G.; Bellani, Giacomo; Winkler, Tilo; Schroeder, Tobias; Petersen, Bodil; Harris, R. Scott; Melo, Marcos F. Vidal

doi:10.1097/01.anes.0000264748.86145.ac

Cited by 88 publications

(140 citation statements)

References 60 publications

(85 reference statements)

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“…Under the assumption of steady state conditions, the 18 F-FDG distribution volume of the precursor compartment as a fraction of lung volume (F e ), can be derived as (3) which is effectively the same equation as the one used to derive F e from the rate constants of the Sokoloff model (14). The corresponding fractional 18 F-FDG distribution volume of the extravascular/non-cellular compartment (F ee ) is given by (4) The net uptake rate K i was derived from the estimates of the individual rate constants as (5) where right side is identical to the corresponding equation used for the Sokoloff model (14).…”

Section: Model Of Lung 18 F-fdg Kinetics During Acute Lung Injury: Twmentioning

confidence: 99%

“…We re-analyzed 18 F-FDG PET imaging and pulmonary arterial blood sampling data from previous studies on lung inflammation in sheep (4,6). These studies included 5 sheep exposed to unilateral cigarette smoke inhalation (smoke group) (6) and 10 sheep exposed to unilateral injurious ventilation (4), 6 of which with negative end-expiratory pressure of −10 cm H 2 O (NEEP group), and 4 of which with positive end-expiratory pressure of 10 cm H 2 O (PEEP group).…”

Section: Experimental Datamentioning

confidence: 99%

“…Recently, PET imaging of the glucose analog 2-deoxy-2-[ 18 F]fluoro-D-glucose ( 18 F-FDG), a standard tool in oncology, is increasingly used to assess metabolic activity of pulmonary inflammatory cells (4)(5)(6)(7)(8)(9)(10)(11). Such measurement is based on the fact that 18 F-FDG is phosphorylated and trapped in activated pulmonary neutrophils in proportion to the cells' glucose uptake, which is much higher than that of lung parenchyma.…”

Section: Introductionmentioning

confidence: 99%

“…There is, however, no consensus about a standard method to quantitatively analyze 18 F-FDG kinetics in the inflamed lung. Some investigators (4,6,8,12) calculated a lung net uptake rate of 18 F-FDG (K i ) using the Patlak method (13,14) and normalized K i by the initial tracer distribution volume (8,12) or by the tissue fraction (4,6) to account for regional differences in lung density. Other investigators (10) considered tracer kinetic modeling with Sokoloff's threecompartment model (15) as the gold standard for analyzing lung 18 F-FDG kinetics.…”

Section: Introductionmentioning

confidence: 99%

“…We analyze previously obtained experimental PET imaging data from sheep with smoke inhalation (6) or ventilator-induced ALI (4) and compare the Sokoloff model against the new lung-specific model in their ability to characterize the pulmonary 18 F-FDG kinetics. Also, we utilize a generalized linear least squares (GLSQ) method (21) to identify the models' parameters instead of the iterative nonlinear curve fitting typically used for this purpose.…”

Section: Introductionmentioning

confidence: 99%

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Modeling Pulmonary Kinetics of 2-Deoxy-2-[18F]fluoro-d-glucose During Acute Lung Injury

et al. 2008

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Rationale and objectives-Dynamic positron-emission tomography (PET) imaging of the radiotracer 2-deoxy-2-[18F]fluoro-D-glucose ( 18 F-FDG) is increasingly used to assess metabolic activity of lung inflammatory cells. To analyze the kinetics of 18 F-FDG in brain and tumor tissues the 'Sokoloff' model has been typically used. In the lungs, however, a high blood-to-parenchymal volume ratio and 18 F-FDG distribution in edematous injured tissue could require a modified model to properly describe 18 F-FDG kinetics.Material and Methods-We developed and validated a new model of lung 18 F-FDG kinetics that includes an extravascular/non-cellular compartment in addition to blood and 18 F-FDG precursor pools for phosphorylation. Parameters obtained from this model were compared with those obtained using the Sokoloff model. We analyzed dynamic PET data from 15 sheep with smoke or ventilatorinduced lung injury.Results-In the majority of injured lungs, the new model provided better fit to the data than the Sokoloff model. Rate of pulmonary 18 F-FDG net uptake and distribution volume in the precursor pool for phosphorylation correlated between the two models (R 2 = 0.98, 0.78), but were overestimated with the Sokoloff model by 17% (p < 0.05) and 16% (p < 0.0005) as compared to the new one. The range of the extravascular/non-cellular 18 F-FDG distribution volumes was up to 13% and 49% of lung tissue volume in smoke and ventilator-induced lung injury, respectively. Conclusion-The lung-specific model predicted 18 F-FDG kinetics during acute lung injury more accurately than the Sokoloff model and may provide new insights in the pathophysiology of lung injury.

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Section: Model Of Lung 18 F-fdg Kinetics During Acute Lung Injury: Twmentioning

confidence: 99%

Section: Experimental Datamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Modeling Pulmonary Kinetics of 2-Deoxy-2-[18F]fluoro-d-glucose During Acute Lung Injury

et al. 2008

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Pulmonary-Respiratory Medicine

2001

JAMA

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Hyperpolarized gas diffusion MRI for the study of atelectasis and acute respiratory distress syndrome

et al. 2014

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Considerable uncertainty remains about the best ventilator strategies for the mitigation of atelectasis and associated airspace stretch in patients with acute respiratory distress syndrome (ARDS). In addition to several immediate physiological effects, atelectasis increases the risk of ventilator-associated lung injury (VALI), which has been shown to significantly worsen ARDS outcomes. A number of lung imaging techniques have made substantial headway in clarifying the mechanisms of atelectasis. This paper reviews the contributions of CT, PET, and conventional MRI to understanding this phenomenon. In doing so, it also reveals several important shortcomings inherent to each of these approaches. Once these shortcomings have been made apparent, we describe how hyperpolarized gas magnetic resonance imaging (HP MRI)—a technique that is uniquely able to assess responses to mechanical ventilation and lung injury in peripheral airspaces—is poised to fill several of these knowledge gaps. The HP-MRI-derived apparent diffusion coefficient (ADC) quantifies the restriction of 3He diffusion by peripheral airspaces, thereby obtaining pulmonary structural information at an extremely small scale. Lastly, this paper reports the results of a series of experiments that measured ADC in mechanically ventilated rats in order to investigate (i) the effect of atelectasis on ventilated airspaces; (ii) the relationship between positive end-expiratory pressure (PEEP), hysteresis, and the dimensions of peripheral airspaces; and (iii) the ability of PEEP and surfactant to reduce airspace dimensions after lung injury. An increase in ADC was found to be a marker of atelectasis-induced overdistension. With recruitment, higher airway pressures were shown to reduce stretch rather than worsen it. Moving forward, HP MRI has significant potential to shed further light on the atelectatic processes that occur during mechanical ventilation.

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Regional Gas Exchange and Cellular Metabolic Activity in Ventilator-induced Lung Injury

Cited by 88 publications

References 60 publications

Modeling Pulmonary Kinetics of 2-Deoxy-2-[18F]fluoro-d-glucose During Acute Lung Injury

Modeling Pulmonary Kinetics of 2-Deoxy-2-[18F]fluoro-d-glucose During Acute Lung Injury

Pulmonary-Respiratory Medicine

Hyperpolarized gas diffusion MRI for the study of atelectasis and acute respiratory distress syndrome

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