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 63 year old woman developed progressive shortness of breath, pulmonary hypertension, and respiratory failure and died from pulmonary fibrosis 45 years after thoracic fistulography with Thorotrast. Bouts of acute respiratory failure occurred with features of noncardiogenic pulmonary oedema. Lung tissue obtained by biopsy and at necropsy showed abundant radioactive particles of thorium dioxide in the lungs. The particles were congregated in the walls of blood vessels and in perivascular fibrous zones, consistent with a causal role of Thorotrast in the development of lung fibrosis. It is suggested that the fibrosis was due to the combined effects of alpha radiation on the interstitial perivascular zones and of recurrent pulmonary oedema due to endothelial damage.
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PMID:Lung fibrosis induced by Thorotrast. 225 23

A smoke inhalation model was created in 22 adult male sheep with pine smoke inhalation through an endotracheal tube for 6 min. Arterial blood gases, HbCO, HbO2 and pulmonary compliance (Cdyn) were monitored, and the morphology of the tracheobronchial tree and pulmonary parenchyma were studied by light and electron microscopy. Severe carbon monoxide poisoning with fatal levels of HbCO (greater than 50 percent) was found at the end of smoke inhalation. Acute respiratory distress, progressive hypoxemia, decreased pulmonary compliance and increased P(A-a)O2 and Qs/QT occurred after injury. Tracheobronchial blockade by pseudomembrane cast, pulmonary edema, atelectasis and necrosis of pulmonary epithelia were demonstrated pathologically. The mechanisms of CO poisoning and ARF are discussed.
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PMID:The pathophysiology of carbon monoxide poisoning and acute respiratory failure in a sheep model with smoke inhalation injury. 230 76

Adoptive immunotherapy with interleukin-2 (IL-2) is associated with a generalized vascular leak syndrome. Pulmonary edema is a common occurrence and is rarely responsible for acute respiratory failure requiring assisted ventilation. The authors have performed a retrospective review of chest radiographs in 19 patients undergoing the priming course of high-dose IL-2 therapy for metastatic melanoma and renal cell carcinoma. This study was primarily designed to evaluate the prevalence and patterns of pulmonary edema and pleural effusions. During the first 5 days of therapy, alveolar edema was identified in 21% (n = 4) and signs of interstitial edema in 53% (n = 10) of patients. Pleural effusions were seen in 42% (n = 8). No patient in this series required assisted ventilation during this period. However, two patients subsequently developed fatal, drug-related myocardial injury. IL-2 toxicity is a well established cause of self-limited, increased-permeability pulmonary edema.
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PMID:Vascular leak syndrome associated with interleukin-2: chest radiographic manifestations. 235 90

Increasing the ratio of tissue oxygen delivery (DO2) to oxygen consumption can improve the survival of critically ill patients, including those with acute respiratory failure. However, under conditions of ventilation/perfusion mismatch, the use of inotropic or vasodilator drugs to augment cardiac output could, in turn, worsen venous admixture. In a canine model of asymmetric oleic acid-induced pulmonary edema, we examined this possibility by studying the effect of 20 and 40-micrograms/kg doses of parenteral nifedipine on oxygenation variables, venous admixture, and intrapulmonary blood flow distribution. After oleic acid injury, nifedipine caused significant increases in cardiac index by 70% as systemic vascular resistance decreased proportionately by 61%. Stroke volume index (SI) and mean pulmonary arterial pressure increased, while venous admixture and the distribution of intrapulmonary blood flow did not change with nifedipine. However, nifedipine significantly improved the tissue DO2 index so that the coefficient of DO2 increased. Thus, nifedipine significantly increased SI in a dose-dependent manner, thereby improving the tissue oxygen supply-demand balance.
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PMID:Effect of nifedipine on oxygen delivery in canine asymmetric oleic acid lung injury. 236 15

Escherichia coli hemolysin has been implicated as a pathogenicity factor in extraintestinal E. coli infections including sepsis. In the present study the effects of intravascular administration of hemolysin were investigated in isolated blood-free perfused rabbit lungs. Low concentrations of the toxin in the perfusate (0.05-5 hemolytic units/ml, corresponding to approximately 5-500 ng/ml), caused a dose- and time-dependent release of potassium, thromboxane A2, and prostaglandin I2, but not of lactate dehydrogenase, into the recirculating medium, as well as a dose-dependent liberation of the prostanoids into the bronchoalveolar space. These events were paralleled by a dose-dependent pulmonary hypertension, and studies with different inhibitors collectively indicated that the vasoconstrictor response was mediated predominantly by pulmonary thromboxane generation. In addition, E. coli hemolysin elicited a protracted, dose-dependent increase in the lung capillary filtration coefficient, which was independent of the prostanoid-mediated pressor response and resulted in severe pulmonary edema formation. We conclude that E. coli hemolysin can elicit thromboxane-mediated pulmonary hypertension combined with severe vascular leakage in isolated lungs in the absence of circulating inflammatory cells and humoral mediator systems, mimicking the key events in the development of acute respiratory failure in states of septicemia.
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PMID:Thromboxane-mediated hypertension and vascular leakage evoked by low doses of Escherichia coli hemolysin in rabbit lungs. 250 Apr 55

A rare case of chemical burn of the tracheobronchial tree with powdered NaOH in a child is reported. In the course of the disease there were several periods of acute respiratory failure (ARF), requiring respiratory resuscitation with intubation, mechanical ventilation, aspiration and kinesitherapy. The chemical burn was followed by several hours of imaginary well-being, but subsequently pulmonary edema developed. On the fifth day obstruction of the air passages by secretions and mucosal hyperemia led again to acute respiratory failure. On the 15. day bleeding from the mucosa of the respiratory and gastrointestinal tracts developed, which incited again ARF. Such periodic deteriorations, leading to ARF after chemical burns, have been reported in the literature. They require recurrent respiratory resuscitation of different degree and form. Knowledge of these period in the pathologic process, leading to ARF and the adequate respiratory resuscitation are prerequisite for a favourable outcome of the morbid process.
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PMID:[A case of chemical burns of the tracheobronchial tree in childhood]. 276 Nov 84

We hypothesized that leukotriene B4 (LTB4) might be produced during endotoxin-induced acute respiratory failure (ARF) observed in young pigs. We used radioimmunoassay (RIA) and reverse phase-high performance liquid chromatography (RP-HPLC) to determine the presence of LTB4 in plasma and bronchoalveolar lavage fluid (BALF) of saline- and endotoxin-treated pigs. Endotoxin was infused at 5 micrograms/kg for 1 hour (hr) followed by 2 micrograms/kg/hr for an average of 3 hrs. Arterial plasma (collected at 0.5 hr intervals for 4 hrs) immunoreactive (i)-LTB4 was significantly increased from 2.5 to 4 hrs of endotoxemia with the peak value occurring at 3.5 hrs (i.e. 282% of baseline value). Analysis of plasma extracts using RP-HPLC revealed an ultraviolet (UV) absorbance peak (270 nm) that was coincident with authentic LTB4 standard. The levels of i-LTB4 were significantly increased in BALF recovered from endotoxemic pigs (337 +/- 71 vs 53 +/- 13 pg/ml for saline controls). Endotoxin also increased the postmortem wet/dry ratio of bloodless lung and BALF albumin concentration, indicating pulmonary edema and increased permeability of the alveolar-capillary membrane, respectively. We conclude that LTB4 is increased in plasma and BALF recovered from endotoxemic pigs and that this lipoxygenase metabolite could possibly be an important factor contributing to the pathophysiology of endotoxin-induced ARF.
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PMID:Increased leukotriene B4 in bronchoalveolar lavage fluid and plasma of endotoxemic pigs. 284 90

The sulfidopeptide leukotrienes (LT) C4 and D4 have been reported to promote the formation of pulmonary edema when administered into the pulmonary circulation of laboratory animals. As a first step in the evaluation of the hypothesis that these leukotrienes participate in the edema formation of the adult respiratory distress syndrome (ARDS), we investigated whether LTC4 and LTD4 were present in the bronchoalveolar lavage (BAL) fluid of patients with ARDS compared to nonsmoker control subjects and to patients with acute respiratory failure exhibiting no radiographic evidence of widespread pulmonary infiltrates but having a clinical predisposition for developing ARDS, i.e., the "at risk" group. Bronchoscopic lavage was performed with sterile 0.9% NaCl on 32 control subjects, nine patients with ARDS, and nine patients "at risk" for ARDS. Leukotrienes were measured in BAL fluid by radioimmunoassay after methanol extraction and HPLC purification of a 20-ml aliquot of the BAL sample. LTC4 and LTD4 (mean +/- SE) increased from 1.1 +/- 0.2 and 1.2 +/- 0.5 ng/lavage in the BAL fluid of control subjects to 6.3 +/- 2.3 and 20.1 +/- 5.9 ng/lavage in patients "at risk" for ARDS and to 12.5 +/- 3.0 and 30.5 +/- 7.8 ng/lavage in patients with ARDS, respectively. The sulfidopeptide LTs correlated with BAL fluid protein content. These results suggest that increased amounts of LTs in BAL fluid are a general finding in patients with ARDS and those "at risk" for ARDS.
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PMID:Increased concentrations of leukotrienes in bronchoalveolar lavage fluid of patients with ARDS or at risk for ARDS. 284 42

Severe falciparum malaria complicated by acute renal failure resulted in very high mortality. Ten patients with acute renal failure from falciparum malaria (infected rbc up to 80%) were continuously dialysed using Tenckhoff peritoneal catheter. Five were oliguric and BUN was maintained between 60 to 80 mg/dl (21.4 to 28.6 mmol/l) by hourly 1 to 1.5 liter dialysate exchange during the acute phase. The peritoneal urea clearance (mean +/- SD) was 12.1 +/- 1.2 ml/min with urea nitrogen removal of 13.4 +/- 2.3 g/day. In nonoliguric cases dialysis was also needed for additional removal of waste products since the remaining renal function could not cope with the hypercatabolic state. Peritoneal glucose absorption (135 to 565 g/day) gave considerable caloric supply without volume load and also contributed to the prevention of hypoglycemia. Varying degree of acute respiratory failure developed in all patients with 5 cases (2 oliguric and 3 nonoliguric) progressing to pulmonary edema. Swan-Ganz catheterization and hemodynamic study suggested the role of increased capillary permeability and volume overload from endogenous water formation in the development of pulmonary complication. Continuous removal of fluid and waste products minimized these problems and may prevent the progression of respiratory failure. One patient died of severe sepsis and the other nine survived. This study showed the beneficial contribution of continuous peritoneal dialysis in the management of acute renal failure from severe falciparum malaria.
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PMID:Continuous peritoneal dialysis in acute renal failure from severe falciparum malaria. 312 24

Acute respiratory failure after hepatic resection, especially in case of concomitant liver dysfunction, is the most troublesome postoperative complication. In order to clarify the pathophysiological mechanism of acute respiratory failure, EVLW (extravascular lung water) was measured by double indicator dilution method in canine model. Mongrel dogs underwent laparotomy and the common bile duct was ligated and divided. After 6 weeks, EVLW was significantly elevated compared with that of normal dogs (p less than 0.05). From 4 hours after 70% hepatic resection dextran-40 was loaded to increase PWP (pulmonary wedge pressure). EVLW was increased accompanying the elevation of PWP in all groups, but in the group with biliary obstruction EVLW was significantly increased for the same elevation of PWP. These results suggest that permeability of pulmonary capillary was highly increased after hepatic resection in biliary obstruction group. Pulmonary edema in this canine model seems to resemble ARDS in human and the pathophysiological mechanism was thought to be related with depression of RES phagocytic function, activation of complement system and pulmonary vascular plugging by aggregates of degenerating granulocytes and endothelial injury. Gabexate mesilate blocked the increase of the lung vascular permeability and was thought to be effective to protect the lung from postoperative acute respiratory failure.
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PMID:[Acute respiratory failure after hepatic resection in canine biliary obstruction model]. 314 48


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