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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary edema and hemorrhage (PEH) was induced in rats by cerebral compression and intraveneous norepinephrine. We used scintiphotographic method to demonstrate the blood volume change in the lung subsequent to the hemodynamic events that cause PEH. A specific isotope, Indium-113m, was chosen for this purpose. The isotope forms large molecular, complex with plasma transferrin (molecular weight of roughly 90,000). It is evenly distributed inside the intravascular space. Normally, the lung showed little radioactivity. After cerebral compression or intravenous norepinephrine, a marked increase in radioactivity of the lung was evident. This indicates an accumulation of blood volume in that area. All the animals developed severe PEH which was proved postmortemly. Findings of the present as well as the previous studies agree with each other and indicate that either cerebral compression or norephinephrine elicits generalized systemic vasoconstriction, causing a shift of large amount of blood into the lung. The hemodynamic changes finally result in pulmonary hypertension and subsequent PEH. The scintiphostographic method may be employed as diagnostic tool when a hypervolemic lung change is suspected. Further quantitative analysis is to be accomplished for a prospective clinical application.
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PMID:A scintiphotographic study of pulmonary edema and hemorrhage induced by cerebral compression and norepinephrine. 102 56

Pulmonary edema is a serious complication of heart failure, but often patients with chronic heart failure resist pulmonary edema despite elevated pulmonary venous pressures. This protection might be a result of decreased pulmonary microvascular permeability. Double-isotope scintigraphy with 113mindium-labeled transferrin and 99mtechnetium-labeled erythrocytes allows noninvasive estimation of pulmonary microvascular permeability; an index of transferrin accumulation is calculated that reflects microvascular permeability. Fourteen patients with severe chronic left ventricular dysfunction were compared with a control group of 15 patients with mild coronary artery disease. In the control group the transferrin accumulation index was 0.35 (range -0.3 to 1.0) x 10(-3)/min, and in patients with heart failure the index was 0.0 (range -1.0 to 0.7) x 10(-3)/min, which was significantly lower (p less than 0.01). The reduction in the transferrin accumulation index correlated weakly with the duration of heart failure (R = -0.5, p less than 0.02). These data indicate reduced protein efflux consistent with a decrease in pulmonary microvascular permeability in patients with severe chronic heart failure. Similar changes have been observed in severe mitral stenosis and may reflect a generalized adaptation to chronic pulmonary venous hypertension.
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PMID:Reduced pulmonary microvascular permeability in severe chronic left heart failure. 161 97

Measurements of the biochemical constituents in the fluid lining of the lung can be used for diagnosing and assessing lung disorders. To facilitate such measurements, a high-performance capillary electrophoresis (HPCE) method has been developed by which the proteins in lung fluid can be analyzed. The lung fluid was obtained by a bronchoalveolar lavage procedure using 48 ml of physiological saline to wash out the lung fluid of rats. The proteins were precipitated from the fluid with 10 volumes of acetone and concentrated by dissolution in 2 ml of water containing 0.2% of trifluoroacetic acid. Aliquots of these samples (5 microliters) were then injected into a Bio-Rad HPE-100 capillary electrophoresis instrument fitted with a 50 cm x 50 microns I.D. coated capillary filled with 0.1 M phosphate buffer (pH 2.5). With phosphate buffer in the outlet electrode chamber (cathode) and water in the inlet electrode chamber (anode), the proteins were loaded into the capillary electrophoretically for 10 s at 10 kV constant voltage. The inlet electrode chamber was then filled with phosphate buffer and HPCE was performed at 8 kV constant voltage. Six major protein fractions were resolved in 35 min, and were detected by UV absorption at 200 nm. The procedure was used to compare the lung fluid proteins of normal untreated rats with those of rats exposed by inhalation to perfluoroisobutylene (PFIB) at a concentration of 100 mg/m3. It was found that PFIB induced pulmonary edema involving a translocation of blood compartment proteins into the lung's alveolar compartment. Comparison of the HPCE fractions with similar fractions obtained by high-performance liquid chromatography confirmed albumin, transferrin and IgG as three major proteins translocated into the alveolar space after PFIB exposure.
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PMID:High-performance capillary electrophoresis of proteins from the fluid lining of the lungs of rats exposed to perfluoroisobutylene. 166 23

Accumulation of radioisotope labelled transferrin in the lungs of guinea pigs was determined with an external detection system. The method is based on the intravascular and extravascular distribution of indium-113m labelled transferrin compared with the intravascular distribution of technetium-99m labelled red blood cells. Guinea pigs were given iloprost, a prostacyclin analogue and potent pulmonary vasodilator, and noradrenaline, a pulmonary vasoconstrictor, in an attempt to increase and decrease respectively the blood volume in the lungs. Neither agent altered transferrin accumulation in the lung by comparison with a saline infusion. Iloprost infused before and after oleic acid infusion reduced macro-molecular leakage when compared with oleic acid alone. These data suggest that the double isotope method can distinguish between hydrostatic and injury induced pulmonary oedema.
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PMID:External detection of pulmonary accumulation of indium-113m labelled transferrin in the guinea pig. 169 94

Endotoxemia and sepsis are common causes of respiratory distress (ARDS), which is characterized by increased pulmonary vascular permeability to plasma proteins resulting in "noncardiac pulmonary edema." The aim of this series was to study the effects of the beta-2 receptor agonist, terbutaline, on plasma extravasation in multiple organs, in sheep exposed to endotoxin shock. A double isotope technique was used and the radioactivity was recorded in different organs (lungs, liver, spleen, kidneys, intestine) by a computerized gamma camera. Tc-99m-labeled erythrocytes were used as a marker for intravascular volume and In-111m-labeled transferrin for tracing extravascular plasma leakage. An organ-transferrin index (organ-TI) was calculated for each organ which corrects for changes in blood distribution. Fourteen sheep were anesthetized and ventilated. After stabilization (t = 0) all animals received E. coli endotoxin 10 micrograms/kg by IV infusion during 30 min. At t = 30, seven animals (group T) received IV infusion of terbutaline, 20 micrograms/kg/hr, during 4 h, while the other seven received normal saline and served as controls (group E). The endotoxin infusion caused an immediate and significant increase in the transferrin index in the lungs and in the liver in both groups. The transferrin index continued to rise in the control group towards the end of the experiment (t = 240), while in group T it reached a maximum 60 min after endotoxin. Four hours after endotoxin the transferrin index was significantly higher in the controls than in the terbutaline treated group, both in the lungs and in the liver (P less than 0.01). No significant changes were recorded in the kidneys or over the intestine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of indium-111-labeled transferrin to study plasma extravasation during endotoxin shock and the effects of the beta-2 agonist terbutaline. 186 67

Patients with rheumatic mitral stenosis often have no pulmonary oedema despite considerably increased pulmonary venous pressure. Pulmonary microvascular permeability was measured non-invasively by a previously validated method of double isotope scintigraphy with indium-113m and technetium-99m. This permits calculation of an index reflecting transferrin efflux and thus, indirectly, the microvascular permeability. Fifteen patients with severe mitral stenosis (defined as valve area less than 1.0 cm2) were compared with a control group of 11 patients with mild coronary artery disease. The permeability index was significantly lower in patients with mitral stenosis than in the control group. Furthermore, the extent of reduction of the permeability index correlated with the severity of mitral stenosis as reflected by the Gorlin valve area. This finding may account for the relative resistance of these patients to pulmonary oedema despite chronic pulmonary venous hypertension.
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PMID:Pulmonary microvascular permeability in patients with severe mitral stenosis. 186 52

We measured extravascular density (EVD) and the pulmonary transcapillary escape rate (PTCER) for 68Ga-transferrin using positron emission tomography in 14 normal volunteers and 29 patients with radiographic infiltrates, including six patients with congestive heart failure (CHF), eight patients with the adult respiratory distress syndrome (ARDS), and 15 patients with focal pneumonia. Contralateral, radiographically normal regions were also evaluated in the patients with focal pneumonia. Mean EVD was elevated in the patients with CHF, ARDS, and pneumonia in regions of radiographic infiltrate compared with values from normal subjects (p less than 0.05), but it was not significantly different among the three patient groups. PTCER in normal subjects and in patients with CHF was not significantly different (21 +/- 11 versus 44 +/- 16 x 10(-4) min-1, respectively, p = NS). PTCER was elevated in regions of infiltrate because of either pneumonia (173 +/- 99) or ARDS (170 +/- 79). PTCER was also elevated in regions contralateral to those with focal infiltrate during pneumonia, even though these regions were radiographically normal and had normal EVD values. These results suggest that PTCER is a sensitive but nonspecific index of abnormal pulmonary vascular permeability, which may be useful for classifying patients in clinical studies of pulmonary edema.
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PMID:A positron emission tomographic comparison of pulmonary vascular permeability during the adult respiratory distress syndrome and pneumonia. 198 72

The pathophysiological mechanism of pulmonary oedema following rapid re-expansion of a collapsed lung is poorly understood. It has been suggested that the period of collapse or subsequent reinflation produces an increase in pulmonary microvascular permeability. To investigate this, the pulmonary accumulation of the plasma protein transferrin was measured by radiolabelling it in vivo with indium-113m. Plasma protein accumulation was calculated after correcting the accumulation of transferrin for changes in intrathoracic blood distribution by simultaneously monitoring technetium-99m labelled red blood cells. Functional images of plasma protein accumulation were constructed for the lung fields on a pixel by pixel basis. Investigations were performed on 14 subjects after drainage of a pleural effusion (n = 9) or evacuation of a pneumothorax (n = 5), and on 11 control subjects. Plasma protein accumulation was greater over the regions of lung re-expansion (-0.1-9.6, mean 2.9 x 10(-3)/min) than over the corresponding region of the contralateral lung (-1.2-0.8, mean 0.01 x 10(-3)/min; p less than 0.001). Patients who had undergone re-expansion procedures also had significantly greater plasma protein accumulation than normal controls. Nine of the 14 patients in the re-expansion group had clearly identifiable areas of increased plasma protein accumulation that corresponded to the part of the lung that had been re-expanded; no regional abnormalities were recorded in the control group. These results suggest that the reinflated lung displays abnormal microvascular permeability.
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PMID:Changes in pulmonary microvascular permeability accompanying re-expansion oedema: evidence from dual isotope scintigraphy. 239 90

A radiographic scoring system has been reported to have a high diagnostic accuracy in the differentiation of pulmonary oedema of renal, cardiac and capillary origin. In the present study, a similar scoring system was used in 51 patients with radiographic appearances of pulmonary oedema due to renal failure (n = 16), cardiac failure (n = 13) and to adult respiratory distress syndrome (ARDS) (n = 22). Evidence of increased pulmonary capillary permeability to transferrin was sought in all patients using a double-isotope method to derive a protein accumulation index (PAI). Using the clinical diagnosis of each type of pulmonary oedema as the "gold standard", sensitivity, specificity and accuracy for the chest radiographic scoring system in pulmonary oedema of cardiac origin were 46, 84 and 75%, respectively. For renal patients these values were 63, 86 and 78% and for ARDS, 89, 33 and 77%. For the PAI in ARDS, sensitivity was 85%, specificity 67% and accuracy 86%. The radiographic scoring system failed to distinguish between pulmonary oedema of renal and cardiac origin and cannot be considered of diagnostic value, but it was more successful in assessment of ARDS. Radiographic appearances suggestive of capillary injury and increased capillary permeability to transferrin occurred in all groups and such findings are not specific to ARDS as currently defined.
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PMID:The radiographic differentiation of pulmonary oedema. 266 83

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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PMID:External 113Inm and 99Tcm radiation detection of lung edema induced by oleic acid in the guinea pig. 322 34


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