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

The pathogenesis of shock lung as well as the success of therapy in this condition was studied in 79 cases of extrathoracic trauma. The water-, hemoglobin-, and DNA contents of the lungs were measured in order to determine the extent of edema, the rate of perfusion, and proliferation. The cases were divided into two groups according to whether they had or had not received medical therapy before death. The data from these two groups were compared using statistical methods in which time of survival was especially taken into account. The fluid balance, pO2, pCO2, central venous pressure, pH of the serum, total serum protein and serum creatinine were also studied in these cases. Results of the study are as follows. Three phases of the posttraumatic syndrome of shock-lung could be distinguished: phase I (initial phase): blood perfusion is increased, edema is beginning to form, and medical treatment has not yet begun. Phase II (early phase = sydrome of early respiratory failure): pulmonary edema is developing rapidly while perfusion is decreasing. Phase III (late phase = syndrome of late respiratory failure): proliferative changes predominante and the edema is still increasing. The mean weight of the lungs was 397 g (s = 170) in phase I, 774 G (S = 361) In phase II, and 1124 g (s = 310) in phase III. The survival times correlated significantly and positively with the amount of water and DNS in the lungs and significantly and negatively to the amount of hemoglobin in the lungs. Thus, increasing pulmonary edema and increasing proliferative changes occurred with decreasing pulmonary perfusion. This correlation was even noted in groups of patients who had not received medical treatment and whose survival times were short. In treated cases, the fluid balance was significantly and negatively correlated to the total serum protein.
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PMID:[Examinations to phenomenon of shock-lung (author's transl)]. 0 60

Pulmonary edema frequently accompanies acute myocardial infarction (MI). We measured pulmonary arterial (PAP), left atrial (LAP), and aortic pressures (AP),lung lymph flow (QL), and clearance of total serum protein and each of eight protein fractions in five anesthetized sheep before and after coronary artery ligation. After a stable base line of 1 h, ligation produced significant increases in LAP, QL, and clearance of total protein and four protein fractions, but no significant changes in PAP, AP, or lymph-to-plasma total protein concentration ratio (CSL/CSP). Variables returned to pre-MI levels within 2 h after occlusion. The ratio of wet to dry lung weight measured 2 h after ligation was within normal limits. Two sheep in which the time course of postligation LAP was duplicated by left atrial balloon inflation showed no change in QL. The QL changes seen cannot be caused by LAP increase alone without substantial decrease in CSL/CSP. Increased QL with high CSL/CSP is typical of increased lung vascular permeability, which is a plausible explanation of our results.
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PMID:Increased lung lymph transport without heart failure after coronary ligation in sheep. 51 87

Effects of intermittent (IPPB) and positive eng-expiratory pressure (PEEP) ventilation on accumulation of pulmonary edema were compared, in dogs, after infusion of oleic acid. Pulmonary extravascular water was approximated as lung thermal volume (LTV), a double indicator method based on differential transit time for simultaneously injected right-to-left conductivity and thermal pulses. LTV was found to be decreased in animals treated with PEEP. The possibility that observed LTV changes reflect only the effect of PEEP on flow distribution, not lung water, was examined by alternating PEEP and IPPB; short-term changes in LTV did not occur. Mean values of other factors influencing pulmonary water transfer, e.g., pulmonary capillary wedge pressure, serum protein, arterial blood gasses, were not significantly different with or without PEEP. It was concluded that, for the oleic acid lesion, PEEP effects a small reduction in the rate of accumulation of pulmonary edema.
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PMID:Lung thermal volume in pulmonary edema: effect of positive end expiratory pressure. 109 68

Sixty-six respiratory disease-free rats, divided into four groups, were exposed to 70% O2 for 1.5, 4, 7, and 10 days and compared with 31 littermates exposed to room air for equal times. Lung surfactant was separated from macrophages and potential serum protein contamination by differential centrifugation of endobronchial washings. In the O2-exposed rats, developing lung edema was demonstrated by decreased dried/fresh lung weight ratio and increased alveolar protein content at 7 and 10 days. At 7 days, lung compliance slope and hysteresis loop area decreased, while critical opening pressure increased. Ultrastructurally, the only abnormality seen was an irregular widening of the alveolar capillary basement membrane on day 10. Alveolar lecithin content decreased slightly during the 10 days exposure, but remained highly saturated, whereas whole lung lecithin content increased. These results suggest that the initial mechanical and morphological alterations in rats exposed to 70% O2 are related to lung edema and are not dependent upon lung surfactant alterations.
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PMID:Early changes in lungs of rats exposed to 70 per cent O2. 117 22

The study aimed to establish whether furosemide given intravenously improved resorption of hydrostatic pulmonary oedema in 14 dogs mechanically ventilated with positive end-expiratory pressure (PEEP). Hydrostatic pulmonary oedema was created by simultaneous inflation of a left atrial balloon and rapid intravenous infusion of isotonic saline. The hydrostatic process was terminated by deflating the balloon and reducing the infusion rate. A PEEP of 10 cmH2O (1.0 kPa) was applied in all animals; in seven, furosemide was administered (diuretic group), 1 mg/kg intravenously as a bolus followed by an infusion of 0.5 mg/kg per hour, while the remaining seven dogs served as a control group. All dogs were studied for a period of 4 h. The extravascular lung water measured with the double indicator dilution technique was 28.3 +/- 3.8 (diuretic group) and 28.2 +/- 6.8 ml/kg (control group) during maximum oedema. It was reduced to 16.4 +/- 2.2 (diuretic group) vs 19.8 +/- 3.7 ml/kg (control group) after 4 h of resorption, P less than 0.05. Postmortem gravimetric values of extravascular lung water were 9.1 +/- 3.4 (diuretic group) vs 12.6 +/- 5.0 g/kg (control group). In the diuretic group the urinary output increased threefold, and haemoglobin and serum protein concentrations were higher than in the control group. There was a significantly greater decrease in cardiac output and central blood volume in the diuretic group. In conclusion, furosemide given intravenously improved lung fluid resorption in hydrostatic pulmonary oedema, probably by increasing the plasma colloid osmotic pressure.
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PMID:Furosemide, when used in combination with positive end-expiratory pressure, facilitates the resorption of extravascular lung water in experimental hydrostatic pulmonary oedema. 176 1

Inhibitors of cytochrome P450, such as SK&F 525-A, prolong the duration of xylazine-ketamine anesthesia and cause pulmonary edema (PE) and death in rats. To determine the cause of PE, Sprague-Dawley rats were given a single dose of xylazine (21 mg/kg, im) alone or in combination with ketamine (45 mg/kg, im) and/or SK&F 525-A (50 mg/kg, ip) and percentage lung to body weight (%LW/BW) ratios (as an indicator of PE) were compared. The results indicated that xylazine caused PE which was independent of ketamine and was enhanced by SK&F 525-A. Subsequently, it was determined that 42 mg/kg xylazine, im, is an optimal edemagenic dose. Xylazine (42 mg/kg, im) increased the %LW/BW ratio as compared to control. Pleural effusion (PLE) of various amounts was observed in 75% of the animals. The pleural fluid to serum protein ratio for xylazine was similar to that obtained for alpha-naphthylthiourea (5 mg/kg, ip). Extensive serous PLE and alveolar edema with hemorrhage were found at necropsy in xylazine-treated rats. Pretreatment with yohimbine (4.2 mg/kg), prazosin (20 mg/kg), tolazoline (20 mg/kg), yohimbine (4.2 mg/kg) plus prazosin (20 mg/kg), atropine (20 mg/kg), dimethyl sulfoxide (DMSO) (7.8 g/kg), allopurinol (50 mg/kg), superoxide dismutase (20,000 U/kg), catalase (20,000 U/kg), BW755C (50 mg/kg), ibuprofen (50 mg/kg), cystathionine (100 mg/kg) plus taurine (100 mg/kg) did not affect the %LW/BW ratio. PLE was increased by yohimbine, yohimbine plus prazosin, and allopurinol, reduced by DMSO, and not changed in other groups. The results indicate that xylazine caused increased-permeability PE characterized by rapid onset, cellular damage and protein-rich pleural fluid. PE may not be mediated by adverse cardiovascular effects of xylazine and oxygen radicals are possibly involved in its etiology.
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PMID:Xylazine-induced pulmonary edema in rats. 190 33

The etiology of edema associated with pulmonary resection was investigated in five patients during the immediate postoperative period. Three patients received pneumonectomy while two patients had one lobe resected. All patients suffered from severe respiratory distress and had x-ray evidence of diffuse interstitial pulmonary edema within 12 hours of surgery. Hemodynamic data were obtained with radial and pulmonary artery catheters. Edema fluid was obtained along with blood samples for simultaneous determination of protein and albumin content. All patients studied had normal or high cardiac output, normal cardiac filling pressures, and edema fluid protein to serum protein ratio of 0.6 or greater suggestive of permeability changes contributing to edema fluid accumulation. Calculated shunt fraction exceeded 25 percent in all patients. Pulmonary edema has been noted in patients following pulmonary resection in the early postoperative period. In patients reviewed here, two factors appeared to be significant. First is an increase in pulmonary capillary pressure associated with passage of a normal to high cardiac output in a reduced volume pulmonary vascular bed. The second factor, as demonstrated by protein content in the edema fluid, is injury to the alveolar capillary membrane.
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PMID:Permeability pulmonary edema following lung resection. 222 69

Pulmonary edema fluid (PEF) and serum (S) were obtained from 14 patients with cardiac pulmonary edema (CPE) and 25 noncardiac pulmonary edema (NCPE) patients. The type of pulmonary edema was based on a clinical classification. The protein content of PEF was not significantly different between CPE (3.89 +/- 0.25 g/dl, mean +/- SEM) and NCPE (4.35 +/- 0.34 g/dl) patients, but the protein content of serum was different (7.18 +/- 0.27 versus 5.13 +/- 0.23, respectively, p less than 0.001). As expected then, the PEF/S ratio was greater in NCPE than in CPE (0.85 +/- 0.06 versus 0.54 +/- 0.03, respectively, p less than 0.05). Thus, differences in the PEF/S ratios in CPE as compared with those in NCPE are independent of mean edema fluid protein content and dependent on differences in serum protein content. PEF and S proteins were separated into 9 fractions of increasing molecular radius by electrophoresis, and fractional concentrations (percent of total protein content) were calculated. The fractional concentrations of these combined fractions of serum proteins were not different between CPE and NCPE. Fractional PEF/S ratios were significantly greater for combined fractions I-III (p less than 0.01) in CPE than in NCPE and significantly less in fractions VII-IX (p less than 0.01). In CPE, a higher percentage of proteins with smaller molecular radii (45 A) enter the airway compartment in part because of higher hydrostatic pressures, whereas in NCPE, larger proteins enter the airways consequent to increased permeability to proteins with molecular radii greater than 72 A.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distribution of proteins in pulmonary edema. The value of fractional concentrations. 295 84

To examine the development of pulmonary edema during experimental renal dysfunction, left atrial pressure was altered in 14 mongrel dogs divided into two groups. Group 1 was composed of seven control animals, and Group 2 was composed of seven animals with surgically induced renal failure (1 week of bilateral ureteral ligation). Data were obtained at two levels of matched transmural pulmonary vascular pressure (defined as mean left atrial pressure less serum protein osmotic pressure). In the animals with renal dysfunction, extravascular lung water (EVLW) (thermal-green dye technique) was higher at moderately (-1 to -2 mm Hg) and severely elevated (11 to 12 mm Hg) vascular driving pressures (11.5 +/- 1.2 cc/kg vs 10.6 +/- 0.8 cc/kg and 14.8 +/- 1.3 cc/kg vs 13.0 +/- 1.9 cc/kg, respectively, both P less than 0.05 vs control). Because protein osmotic pressure was lower in the renal failure group (15.0 +/- 1.8 mm Hg vs 18.4 +/- 1.4 mm Hg, P less than 0.05), greater accumulations of extravascular lung water occurred at lower levels of left atrial pressure (14.2 +/- 1.4 mm Hg vs 17.1 +/- 1.2 mm Hg, P less than 0.05; 26.8 +/- 2.6 mm Hg vs 29.5 +/- 2.3 mm Hg, P less than 0.01). In addition, when the ratio of EVLW/PBV (pulmonary blood volume) was examined in both groups at each stage of the experiment, the ratio was greater in the Group 2 animals at each elevated pressure, suggesting increased permeability with renal dysfunction. In conclusion, pulmonary edema formation occurs at lower left atrial pressures in the setting of sustained renal dysfunction, this phenomenon can be partially explained by lower protein osmotic pressure though altered pulmonary microvascular permeability may contribute to edema formation.
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PMID:Effect of prolonged renal dysfunction on intravascular and extravascular pulmonary fluid volumes during left atrial hypertension. 330 34

We examined the usefulness of serum colloid osmotic pressure measurement in patients with chronic rather than acutely occurring low serum protein concentrations. We used two oncometers, the IL 186 Weil Oncometer and the Wescor Model 4100; results from the two instruments were interchangeable. Values for the colloid osmotic pressure were compared with those for serum total protein (r = 0.783) and albumin concentrations (r = 0.882), which were similar to previously published values. Our day-to-day CV was 2.8%. In studying over 100 patients we found that the previously reported occurrence of pulmonary edema in almost all patients whose colloid osmotic pressure was less than 12.5 mmHg was not seen in the chronic hypoproteinemic patients. We noted only one fatality in our patients whose colloid osmotic pressure was less than 10.5 mmHg, a value found to be associated with fatality in one previous study of acutely ill patients. Factors such as ambulation, fasting, dehydration, and the nature of the blood sample can markedly affect the value for colloid osmotic pressure value, and this, coupled with the good correlation with the serum albumin in several studies, leads us to question the usefulness of measuring colloid osmotic pressure in a non-specialist hospital environment, either as an adjunct to the measurement of serum protein or albumin, or as an independent test.
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PMID:Measurements of serum colloid osmotic pressure are of limited usefulness. 705 98


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