Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A severe upper respiratory disease of young turkeys is described that resulted in high morbidity and mortality. Death was due to asphyxiation produced by occlusion of the trachea or nostrils. The postmortem lesions were tracheitis, pulmonary edema, swollen livers and spleens, and a drastic reduction in bursa size. Bursal necrosis and loss of tracheal epithelium were found in tissue sections from clinically affected birds. Antibody to infectious bursal disease was found by agar-gel precipitin and virus-neutralization tests of serum samples from affected flocks. A geometric mean titer of 31.5 for Newcastle disease was found in unvaccinated flocks of five-week-old turkeys.
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PMID:Rhinotracheitis in turkey poults. 21 6

3-Methylindole, a ruminal fermentation product of tryptophan, induces acute pulmonary edema and emphysema in cattle, and 3-methylindole is present in the ruminal fluid and blood of cows with a natually occurring form of this disease. Monensin, a polyether antibiotic and widely used feed additive for beef cattle, prevented tryptophan-induced acute bovine pulmonary edema and emphysema. Monensin acted by reducing the ruminal conversion of L-tryptophan to 3-methylindole both in vitro and in vivo. Lasalocid, also a polyether antibiotic, showed similar effects in vitro. These results provide a promising approach to prevention of this major respiratory disease of cattle.
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PMID:Monensin and the prevention of tryptophan-induced acute bovine pulmonary edema and emphysema. 66 43

Intraruminal and intravenous administration of 3-methylindole (3MI; skatole) caused interstitial pulmonary edema and emphysema in cattle. In 3 adult heifers given the intraruminal dose of 0.2 g of 3 MI per kilogram of body weight, clinical signs of respiratory disease appeared between 6 and 12 hours after dosing, and death due to pulmonary edema and emphysema occurred at 33, 69, and 72 hours. The mean plasma concentration of 3MI became maximal (18.5 mug/ml) at 3 hours and then decreased to low concentrations by 48 hours. In 2 heifers given an intraruminal dose of 0.1 g of 3MI/kg, clinical signs developed, but they did not die during the 96-hour experiment. The mean plasma concentration of 3 MI became maximal (16.8 mug/ml) at 3 hours and decreased to 1.6 and 0.4 mug/ml at 12 and 36 hours, respectively. At necropsy of the heifers, the lung were large, firm, dark red, and heavier than normal. Diffuse pulmonary edema was the predominant change in cattle which died early, and interstitial emphysema was more severe at later stages of the disease. During the early stages, alveoli were overdistended, and a few more ruptured. Most alveolar spaces were filled with proteinaceous residue, but the alveolar septums were smooth and of normal thickness. At later stages, proliferation of alveolar cells was observed, and alveolar septums were thickened. In 3 cows given 0.06 g of 3MI/kg by jugular infusion, clinical signs appeared in all cows, and 1 cow died of pulmonary edema and emphysema 56 hours after the infusion was started. Severe pulmonary lesions seen in all of the cows given a 3MI infusion were similar to those in the cows given an intraruminal dose of 3MI. The mean plasma concentration of 3MI increased to 10.7 mug/ml at 9 hours after starting the infusion and decreased to 0.5 mug/ml at 18 hours. The results indicate that 3MI, a product of ruminal tryptophan fermentation, can cause pulmonary edema and interstitial emphysema in cattle and support the hypothesis that 3MI is the causative agent in tryptophan-induced pulmonary disease.
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PMID:Pulmonary edema and emphysema in cattle after intraruminal and intravenous administration of 3-methylindole. 116 73

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

Thirty-two consecutive preterm infants with birth weights under 1,500 grams and with respiratory distress syndrome (RDS) complicated by a patent ductus arteriosus (PDA) underwent ligation of PDA. The indications for operation were massive left-to-right shunting associated with heart failure (cardiomegaly and pulmonary edema) unresponsive to medical treatment. The clinical manifestations of heart failure were related to the severity of RDS. Infants with mild-to-moderate RDS (21) often recovered and later developed typical findings of PDA (bounding pulses, hyperactive precordium, and murmur). They are now operated upon as soon as respiratory support is required. Infants with severe RDS (11) develop cardiomegaly earlier, and retrograde aortography may show massive left-to-right shunting before the presence of a murmur. Ligation is indicated when blood-gas values deteriorate despite medical treatment. Nineteen (59 per cent) of these extremely preterm infants survived to be discharged and 16 (50 per cent) are developing normally. Three have neurologic impariment. None of the survivors has clinical respiratory disease, and their radiologic findings of bronchopulmonary dysplasia are improving.
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PMID:Improving the results of ligation of patent ductus arteriosus in small preterm infants. 124 41

The purpose of this study was to see if lung vascular protein permeability is greater in preterm lambs with respiratory distress than it is in lambs without lung disease. We measured pulmonary vascular pressures, lung lymph flow, and concentrations of protein in lymph and plasma of 10 chronically catheterized preterm lambs (gestation 133 +/- 1 d) for 2-4 h before and for 4-8 h after delivery by cesarean section. All lambs were treated with mechanical ventilation after birth and received a constant intravenous infusion of glucose-saline solution at an hourly rate of 10 ml/kg. Respiratory failure developed in six lambs, in which there was a sustained threefold postnatal increase in lung lymph flow and lymph protein flow, with an even greater increase in pleural liquid drainage. Concentrations of protein in lymph and pleural liquid were almost identical, averaging approximately 75% of the plasma protein concentration. In the four preterm lambs without lung disease, lymph flow and lymph protein flow were either near or below fetal values by 6-8 h after birth, and there was little or no pleural liquid drainage. Extravascular lung water averaged 7.3 +/- .8 g/g dry lung in lambs with respiratory failure compared to 4.8 +/- .5 g/g dry lung in lambs without lung disease. Thus, pulmonary edema with abnormal leakage of protein-rich liquid from the lung microcirculation into the interstitium is an important pathological feature of the respiratory disease that often occurs after premature birth.
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PMID:Lung fluid balance in lambs before and after premature birth. 276 Feb 1

The adult respiratory disease syndrome is associated with multiple disorders. At least one of the rickettsial diseases, RMSF, has been reported to be associated with noncardiogenic pulmonary edema. We report herein another rickettsial disease, boutonneuse fever, which is produced by Rickettsia conorii and is usually a mild disease, that in our patient was associated with ARDS.
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PMID:ARDS associated with boutonneuse fever. 292 29

Although pneumonia virus of mice (PVM) is ubiquitous among rodent colonies in the United States, it has not been reported to cause clinically apparent disease in euthymic mice. However, PVM has been reported to cause respiratory disease and death in experimentally infected euthymic and athymic mice. A group of nu/nu mice, housed in quarantine in a Trexler-type isolator, had weight loss and dyspnea. Gross necropsy findings included cachexia and diffuse pulmonary edema or lobar consolidation. Histologically there was diffuse interstitial pneumonia. Electron microscopy revealed filamentous virions budding from plasma membranes, and immunohistochemical staining of lung tissue was positive for PVM antigen. PVM was isolated from affected lung tissue in BHK 21 cells and mouse antibody production tests resulted in seroconversion to PVM. Experimental inoculation of athymic mice with lung homogenate from spontaneously infected mice resulted in clinically apparent respiratory disease and histologic lung changes similar to those in naturally infected mice. Inoculation of athymic mice with infected BHK 21 cell culture fluid resulted in pneumonia which was qualitatively similar to, but less severe than, that observed in mice with spontaneous disease. These findings indicate that naturally occurring PVM infection in athymic mice may cause respiratory disease and wasting.
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PMID:Respiratory disease and wasting in athymic mice infected with pneumonia virus of mice. 337 86

Plasma colloid osmotic pressure (COP) was measured in three groups of very low birthweight infants. Babies in Group 1 (n = 8) were breathing spontaneously and had no respiratory disease. Those in Group 2 (n = 9) received assisted ventilation for hyaline membrane disease (HMD), and those in Group 3 (n = 7) received assisted ventilation for other reasons (five apnoea, two pneumonia). Both assisted ventilation groups had lower mean COP values than spontaneously breathing infants. Mean values (s.e.m.) for Groups 1, 2 and 3, respectively, were: 15.3 (0.6), 11.3 (0.4) and 11.9 mmHg (0.5) (P less than 0.001) on Day 1; and 15.2 (0.4), 12.9 (0.4) and 12.8 mmHg (0.3) (P less than 0.001) on Day 2. The increase from Day 1 to Day 2 was significant for those with HMD (P less than 0.05). Colloid osmotic pressure correlated with mean blood pressure (r = 0.51; P less than 0.001) but not with birthweight, gestation, crystalloid fluid intake or pH. The role of low COP in the pathogenesis of acute respiratory failure in infants with uncomplicated HMD is unclear, but such low COP may contribute to development of pulmonary oedema as a complication, particularly if the ductus arteriosus is still patent and the infants are given high volume intravenous fluids.
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PMID:Low colloid osmotic pressure in very low birthweight infants receiving assisted ventilation. 366 82

In the present study we investigated the phospholipid composition of small-volume (up to 20 ml) in vivo bronchoalveolar lavage and that of quantitative ex vivo bronchoalveolar lavage. Furthermore, the accuracy of the small-volume lavage in predicting lung disease was evaluated. There was a positive linear correlation (r approximately equal to 0.87-0.91) between the amount of saturated phosphatidylcholine and the saturated phosphatidylcholine/sphingomyelin ratio in quantitative bronchoalveolar lavage. The phospholipid distributions in the small-volume lavage and the quantitative lavage were similar (r approximately equal to 0.78-0.94, n = 14). The overall accuracy of phosphatidylcholine/sphingomyelin ratio and phosphatidylglycerol/total phospholipid ratio in predicting the presence or absence of respiratory failure was 85-87% in newborns, children, and adults. In respiratory diseases without respiratory failure, the abnormalities in the phospholipids were frequent, although less distinct. According to animal experiments the surfactant system is inhibited at the onset of high permeability lung edema. Soon thereafter, the lavageable surfactant pool is decreased. Present findings support the view that surfactant defects are of importance in the pathogenesis of respiratory disease, and that surfactant-oriented therapy may be effective in the treatment and prevention of respiratory failure.
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PMID:Endobronchial surface active phospholipids in various pulmonary diseases. 386 Mar 95


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