Single Isotope Evaluation of Pulmonary Capillary Protein Leak (ARDS Model) Using Computerized Gamma Scintigraphy

Tatum, James L.; Strash, Alfred M.; Sugerman, Harvey J.; Hirsch, Jerry I.; Beachley, Michael C.; Greenfield, Lazar J.

doi:10.1097/00004424-198111000-00004

Cited by 12 publications

(4 citation statements)

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“…This indicates a role of endogenously produced oleic acid in lung edema, although the oleic acid in this investigation was used primarily as an experimental tool. The results from the external radiation detection with increasing leak-index slope after additional oleic acid treatment is in agreement with previously reported results [16]. The leak-index slope is of the same magnitude as reported by Dauber et al [4].…”

Section: Discussionsupporting

confidence: 93%

“…Gorin et al [6] described a sheep model in which experimentally induced lung edema was measured with the aid of a radioisotope tracer technique and an external gamma radiation detector with continuous sampling. The basic ideas of that work have been used by others after modification of experimental procedures and calculations [1,4,15,16]. This paper deals with miniaturized radiation detector equipment and an experimental set-up for use in guinea pigs.…”

Section: Introductionmentioning

confidence: 99%

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External113Inm and99Tcm radiation detection of lung edema induced by oleic acid in the guinea pig

Hultkvist

Bjellin

Mårtensson³

1988

Res. Exp. Med.

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The establishment of a small animal model for studies of lung injury is in great demand. Therefore, a double radioisotope labeling method was applied to study the dynamics of lung injury with protein-rich edema in the anesthetized guinea pig. One external scintillation detector was placed over the lung and another over the heart, where they continuously sampled the energy spectrum of 113Inm labeled transferrin, a macromolecular marker, and 99Tcm labeled red blood cells (RBC), a blood pool marker. Lung injury was induced by i.v. oleic acid in doses of 0.03 and 0.06 ml/kg b.wt. infused for 10 min. We calculated the rate of increase of accumulated 113Inm-transferrin in the lung corrected for blood pool changes. Macromolecular leakage showed a graded response in regression line-slope (RLS) to oleic acid. Both oleic acid groups showed significantly different RLSs as compared to the saline control (mean +/- SD x 10(-3) min-1; 0.03 ml: 3.86 +/- 1.01 (n = 7); 0.06 ml: 10.75 +/- 4.06 (n = 6), and control 1.12 +/- 1.19 (n = 6]. Assays of changes of acid-base balance, cell dynamics, and lung wet-dry weight were in accordance with the occurrence of lung edema. The RLS was well correlated with the lung wet-dry weight (r = 0.98). We conclude that measurements of pulmonary edema in guinea pigs can be performed quantitatively with the aid of external detection of radiolabeled transferrin and RBC:s. Thus, the method could be useful in further studies on mechanisms and/or treatment of protein-rich lung edema.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

External113Inm and99Tcm radiation detection of lung edema induced by oleic acid in the guinea pig

Hultkvist

Bjellin

Mårtensson³

1988

Res. Exp. Med.

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“…This technique could not be used here as we used 99m Tcalbumin for our double-isotope imaging of protein fluxes across the alveolo-capillary barrier. We then used the normalized lung-to-heart ratio slope of 111 In-transferrin that is related to the normalized slope index in the absence of lung and blood volume change (41,47,49). We already showed that the 111 In-transferrin lung-to-heart ratio slope correlates well with protein accumulation rate in lungs during ventilator-induced lung injury (6).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of two-way protein fluxes across the alveolo-capillary membrane by scintigraphy in rats: effect of lung inflation

Prost

Dreyfuss²,

Saumon³

2007

Journal of Applied Physiology

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Pulmonary microvascular and alveolar epithelial permeability were evaluated in vivo by scintigraphic imaging during lung distension. A zone of alveolar flooding was made by instilling a solution containing 99mTc-albumin in a bronchus. Alveolar epithelial permeability was estimated from the rate at which this tracer left the lungs. Microvascular permeability was simultaneously estimated measuring the accumulation of (111)In-transferrin in lungs. Four levels of lung distension (corresponding to 15, 20, 25, and 30 cmH2O end-inspiratory airway pressure) were studied during mechanical ventilation. Computed tomography scans showed that the zone of alveolar flooding underwent the same distension as the contralateral lung during inflation with gas. Increasing lung tissue stretch by ventilation at high airway pressure immediately increased microvascular, but also alveolar epithelial, permeability to proteins. The same end-inspiratory pressure threshold (between 20 and 25 cmH2O) was observed for epithelial and endothelial permeability changes, which corresponded to a tidal volume between 13.7 +/- 4.69 and 22.2 +/- 2.12 ml/kg body wt. Whereas protein flux from plasma to alveolar space ((111)In-transferrin lung-to-heart ratio slope) was constant over 120 min, the rate at which 99mTc-albumin left air spaces decreased with time. This pattern can be explained by changes in alveolar permeability with time or by a compartment model including an intermediate interstitial space.

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“…Roselli et al finally simplified and homogenized this technique by validating the normalized slope index, that is, "the time rate of change of radioactivity originating from protein in lung interstitium divided by this ratio at time 0, and corrected for blood volume changes". Only one tracer could be used providing the decrease of its plasma activity over time would be accounted for by measuring the activity of a fixed plasma volume at different time points and then normalizing the detector count rate by the plasma count rate [47,48] or by selecting a vascular region with a gamma camera in order to quantify plasma protein clearance without the need for a blood sample [49][50][51].…”

Section: Imaging Of Pulmonary Microvascular Permeabilitymentioning

confidence: 99%

Real Time Lung Imaging for the Detection of Lung Injury and Alveolar Fluid Movement During Mechanical Ventilation

Prost¹,

Ricard²,

Saumon³

et al. 2010

TONMEDJ

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Experimental ventilator-induced lung injury (VILI) is characterized by alterations in alveolar epithelial and microvascular permeability that favors the systemic dissemination of lung borne cytokines or bacteria. Animal models of VILI have been shown relevant to patient care and outcome and help explaining why most patients with the acute respiratory distress syndrome do not die from respiratory failure but from multiple organ dysfunction. Recent experimental studies also showed that adverse ventilator patterns may propel airway secretions and bacteria to previously healthy lung regions. Noninvasive imaging techniques were used for years to study the net rate of protein flow across the pulmonary microvascular endothelium and the alveolar epithelium in vivo, during normal breathing and lung inflation. More recently, the two-way protein fluxes across the alveolo-capillary barrier and the intra-pulmonary dispersion of alveolar edema have been monitored during mechanical ventilation. These experiments have provided new insights on the mechanisms of experimental VILI that may be of clinical value. This review will describe the evolution of these techniques and their main physiological and pharmacological applications in the era of VILI.

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Single Isotope Evaluation of Pulmonary Capillary Protein Leak (ARDS Model) Using Computerized Gamma Scintigraphy

Cited by 12 publications

References 0 publications

External113Inm and99Tcm radiation detection of lung edema induced by oleic acid in the guinea pig

External113Inm and99Tcm radiation detection of lung edema induced by oleic acid in the guinea pig

Evaluation of two-way protein fluxes across the alveolo-capillary membrane by scintigraphy in rats: effect of lung inflation

Real Time Lung Imaging for the Detection of Lung Injury and Alveolar Fluid Movement During Mechanical Ventilation

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