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

A 48-year-old man with small cell lung cancer developed ARDS, and massive pulmonary edema fluid was obtained with the fiberoptic bronchoscopy. The pulmonary edema fluid to serum ratios of total protein and albumin were 0.72 and 0.85 respectively. The ratio of LDH was higher (2.71), while that of cholesterol was lower (0.11) than that of total protein. Simultaneously, isopropyl N [I-123] p iodoamphetamine (I-123 IMP) and I-131 human serum albumin (I-131 HSA) were injected into this patient. Samples of blood and pulmonary edema fluid were collected to measure the clearance through the pulmonary microvasculature. The time activity curves of I-123 IMP and I-131 HSA in his blood samples revealed almost constant radioactivity from 5 minutes to 120 minutes after injection, while both radioactivity levels in pulmonary edema fluid samples increased with time. The clearance ratio of I-123 IMP to I-131 HSA was constant at each sampling time (mean +/- SD, 1.51 +/- 0.32). The linear correlation between I-123 IMP clearance and I-131 HSA clearance (r = 0.95, p less than 0.01) suggested that the clearance ratio of exudative plasma components may remain unchanged even if pulmonary microvasculature permeability has changed.
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PMID:[Assessment of the permeability of the pulmonary microvasculature using radiotracers in a case of adult respiratory distress syndrome]. 185 5

Similarities between oleic acid (OA)-induced pulmonary injury and clinical adult respiratory distress syndrome (ARDS) have resulted in extensive use of this model. Using technetium 99m (Tc-99m)-labeled human serum albumin (Tc-HSA) we examined the effect of indomethacin (a prostaglandin synthetase inhibitor) and dexamethasone (a corticosteroid) alone and in combination on OA-induced pulmonary protein leak. Computer-acquired dynamic gamma camera imaging before (15 min), during, and after (60 min) OA infusion were used to generate time-activity curves for lung and heart regions. A lung:heart activity ratio curve with a positive slope indicates pulmonary capillary protein leak of the labeled substance. Tc-99m labeling of red blood cells followed by OA injury showed no significant change in slope, indicating that lung hemorrhage was not being measured; however, Tc-HSA showed significant protein leakage following OA injury. Pretreatment with indomethacin or dexamethasone did not significantly alter either the preinsult or the postinsult slope. Combined pretreatment with indomethacin and dexamethasone significantly decreased, but did not eliminate, the pulmonary protein leak produced by OA injury. Our results indicate that multiple factors are involved in the production of the pulmonary capillary leak in OA-induced lung injury. In addition to the possible therapeutic efficacy of combined corticosteroids and nonsteroidal antiinflammatory drugs, our results demonstrate that these substances may be useful in defining the pathophysiology involved in permeability pulmonary edema.
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PMID:Indomethacin and dexamethasone decrease oleic acid-induced pulmonary protein leak in rabbits. 380 24

Nuclear medicine imaging procedures can play a significant role in evaluating the pulmonary complications that are seen in trauma patients. A quantitative method for measuring increased pulmonary capillary permeability that uses Tc-99m HSA allows early diagnosis of acute respiratory distress syndrome (ARDS) and accurately differentiates this condition from pneumonia or cardiogenic pulmonary edema. This technique may be of great value in following the response to therapy. The use of 133Xe to diagnose inhalation injury remains an important diagnostic tool, particularly at hospitals with specialized burn units. Regional decreases in ventilation-perfusion images reliably localize aspirated foreign bodies. Radionuclide techniques that are used to demonstrate gastropulmonary aspiration remain controversial and require further clinical evaluation. Pulmonary perfusion imaging, although nonspecific, may provide the earliest clue for correct diagnosis of fat embolism, air embolism, contusion, or laceration. Furthermore, the possibility of perfusion abnormality due to these uncommon conditions must be remembered whenever trauma patients are evaluated for pulmonary thromboembolism with scintigraphy. Occasionally, liver or spleen scintigraphy may be the most appropriate procedure when penetrating chest trauma also involves these subdiaphragmatic organs.
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PMID:Radionuclide evaluation of lung trauma. 622 97

Computerized gamma scintigraphy revealed a significant (p less than 0.001) rising lung:heart radioactivity ratio, which has been called "slope of injury" or "slope index", with both 99mTechnetium-tagged human serum albumin (99mTc-HSA) and 99mTechnetium-tagged red blood cells (99Tc-RBC) after 0.05 or 0.2 ml/kg iv oleic acid administration to dogs. This slope index was significantly greater with 99mTc-HSA than 99mTc-RBC (p less than 0.001). These findings verify that the scintigraphic 99mTc-HSA slope of injury is a result of a pulmonary capillary protein leak and not oleic acid induced changes in pulmonary blood or air volume. The leak of red blood cells noted with scintigraphy was confirmed by light microscopy and examination of the tracheal edema fluid. The leak of albumin, however, was much greater than the leak of red blood cells by microscopy and tracheal fluid examination, confirming the scintigraphic data. This study provides further evidence that computerized gamma scintigraphy will be of value for the diagnosis of permeability pulmonary edema and its response to treatment.
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PMID:Comparative scintigraphy in oleic acid pulmonary microvascular injury. 645 10

To assess the importance of the intravascular Starling forces on the pulmonary microvascular flux of solutes in ARDS, the clearance from blood to pulmonary edema fluid of a small-molecular-weight hydrophilic radiotracer, indium-111-DTPA, and a large-molecular-weight radiotracer, iodine-125-HSA, in patients with noncardiac pulmonary edema was measured. Since permeability changes of the pulmonary microvessels in ARDS are likely not homogeneous, the severity of the permeability lesion according to the magnitude of I-HSA flux was predefined. A significant positive correlation between the clearance of In-DTPA and the Pmv-pi mv gradient was found both in patients with a "moderate" (R2 = 0.46, P less than 0.01) and "severe" (R2 = 0.45 P less than 0.01) increase in microvascular permeability. The clearance of I-HSA from blood to edema fluid was also positively correlated with the Pmv and the Pmv-pi gradient. Therefore, even though ARDS is primarily characterized by a spectrum of change in permeability within the pulmonary microvasculature, the flux of both small- and large-molecular-weight solutes remains synergistically modulated by the measurable intravascular Starling forces.
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PMID:The synergistic influence of the intravascular starling forces on pulmonary microvascular solute flux in human ARDS. 674 32

We measured the clearance from blood to pulmonary edema fluid of a small molecular weight hydrophilic radiotracer, Indium-111-DTPA (In-DTPA) and a larger molecular weight radiotracer, Iodine-125-HSA (I-HSA), in patients with pulmonary edema on either a cardiac or noncardiac (permeability) basis. In previous investigations, we had noted an apparent relationship between the magnitude of clearance of I-HSA across the alveolocapillary membrane and the severity of noncardiac pulmonary edema. In this study, we were able to distinguish at least 2 distinct groups of patients with noncardiac pulmonary edema. Patients with the greatest damage to the alveolo-capillary exchanging membrane, defined by the flux of I-HSA from blood to edema fluid, were significantly differentiated from those with a lesser microvascular injury on the basis of higher mean heart rate (HR), temperature, cardiac index (CI), pulmonary artery pressures, right ventricular stroke work index (RVSWI), and a lower mean total white blood cell count (WBC), among others. Therefore, noncardiac pulmonary edema is characterized by a spectrum of permeability injury to the pulmonary microvasculature which seems to parallel other measurable indices of the severity of the systemic response to the illness.
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PMID:Clinical correlates of the spectrum of lung microvascular injury in human noncardiac edema. 682 83

Endotoxemia leads to the induction of inducible nitric oxide synthase (NOS-2) and increased expression of numerous inflammatory mediators contributing to endotoxin-induced acute lung injury. We tested the hypothesis that supplementation of nitric oxide (NO) by the novel NO donor S-nitroso human serum albumin (S-NO-HSA) given after lipopolysaccharide (LPS) challenge may reduce NOS-2 expression, lung inflammation and acute lung injury. Rats were divided into four groups: sham-operated (no treatment), LPS, LPS+HSA (human serum albumin), and LPS+S-NO-HSA. LPS was administered intravenously (20 mg kg(-1)) resulting in acute lung injury and a high mortality rate within 6 h (>90%). LPS-induced lung injury was characterized by an increased lung edema (lung wet/dry weight ratio), pulmonary neutrophil infiltration (myeloperoxidase activity, MPO) as well as a robust inflammatory response [increased expression of intercellular adhesion molecule-1 (ICAM-1), NOS-2, and cyclooxygenase-2 (COX-2)]. Infusion of S-NO-HSA or HSA was started 2 h after LPS and continued for 4 h (total dose of 72 mg kg(-1)) at a rate of 300 microg kg(-1) min(-1). S-NO-HSA but not HSA prolonged survival of endotoxemic rats, reduced the hypotensive response to LPS, minimized LPS-induced lung edema and injury, normalized MPO activity as well as diminished lung expression of pro-inflammatory molecules such as ICAM-1, NOS-2, and COX-2. Continuous supplementation of NO by S-NO-HSA after LPS challenge prevents induction of NOS-2, provides significant protection of endotoxin-induced acute lung injury, and prevents early mortality in endotoxic shock in rats. Our results suggest a potential therapeutic role for S-NO-HSA in endotoxemia.
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PMID:S-nitroso human serum albumin given after LPS challenge reduces acute lung injury and prolongs survival in a rat model of endotoxemia. 1885 85