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

Fumonisin B1 (FB1), a recently identified mycotoxin produced by Fusarium moniliforme in corn, has been shown to cause death in swine due to pulmonary edema, an apparently species specific effect, and to interfere with sphingolipid metabolism in vitro. Here we characterize the toxicity of fumonisins, using female cross-bred swine weighing 6 to 13 kg, and present a hypothesis regarding the mechanism of fumonisin-induced pulmonary edema in swine. FB1 was given daily intravenously (IV) to pig 1 for 9 days for a total of 72 mg (7.9 mg/kg) and to pig 2 for 4 days for a total of 67 mg (4.6 mg/kg). Pig 3 (control) was given saline IV for 9 days. Corn screenings naturally contaminated with FB1 (166 ppm) and FB2 (48 ppm) were fed to pigs 4, 5, and 6, and ground corn was fed to pigs 7 and 8 (controls). Pigs 4 and 7 were killed on day 5; pig 5 was found dead on day 6; and pigs 6 and 8 were killed on day 15. Pigs 4 and 5 had ingested 187 and 176 mg total fumonisins, respectively, while pig 6 had ingested 645 mg. Feed consumption had decreased in pigs fed corn screenings, with an additional sharp decrease prior to onset of clinical signs. Increases in serum liver enzymes, total bilirubin, and cholesterol were present, but electrocardiograms, heart rate, and body temperature were unaffected. Pigs dosed IV with FB1, developed mild intermittent respiratory abnormalities, while those fed screenings developed respiratory distress within 5 days. Mild interstitial pulmonary edema was observed in pig 1. Severe interstitial pulmonary edema, pleural effusion, and increased lung wet/dry weight ratio were observed in pigs 4 and 5. All pigs given fumonisin (either IV or orally) had hepatic changes characterized by hepatocyte disorganization and necrosis; pancreatic acinar cell degeneration was also observed. Ultrastructural changes in orally dosed swine included loss of sinusoidal hepatocyte microvilli; membranous material in hepatic sinusoids; and multilamellar bodies in hepatocytes, Kupffer cells, pancreatic acinar cells and pulmonary macrophages. Pulmonary intravascular macrophages (PIMs) contained large amounts of membranous material. Thus, the target organs of fumonisin in the pig are the lung, liver, and pancreas. At lower doses, slowly progressive hepatic disease is the most prominent feature, while at higher doses, acute pulmonary edema is superimposed on hepatic injury and may cause death. We hypothesize that altered sphingolipid metabolism causes hepatocellular damage resulting in release of membranous material into the circulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Characterization of fumonisin toxicity in orally and intravenously dosed swine. 138 61

Physiological and pathological respiratory responses are triggered by various conditions of exposure to cold climates. Beside airway smooth muscle, both the pulmonary and the tracheobronchial vasculatures are major effectors of respiratory responses to cold. General exposure to cold causes pulmonary vasoconstriction known as "Raynaud's phenomenon of the lung" in subjects with primary Raynaud syndrome and favors acute pulmonary oedema in subjects with congestive heart failure. In healthy subjects acute hyperventilation of very cold air has led to acute respiratory failure closely similar to hypoxic pulmonary oedema. In outdoor exercising people years long repetition of hyperventilation of subfreezing air causes "eskimo lung" made of obstructive lung disease and increased wall thickness of pulmonary arteries. At a lesser degree hyperventilation of dry air cools the central airways and triggers subclinical bronchial obstruction in healthy subjects. In asthmatic subjects hyperventilation of dry air causes asthma attacks. Results of recent animal and human experiments point to a key role of mucosal vessels in thermal balance of the airways. Simultaneously, there is increasing evidence that hyperventilation-induced asthma is triggered by a thermal stimulus.
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PMID:Cold and the airways. 148 69

Four adults and a child undergoing surgery with sevoflurane anesthesia developed acute pulmonary edema immediately after anesthesia. Prior to development of pulmonary edema all patients exhibited severe arterial hypertension and tachycardia. Their episodes of circulatory changes were, we believed, caused by the local injection of epinephrine for hemostasis in 2 patients (9 y.o. child, 45 y.o. man) and the intrusion of painful surgical stimuli in one patient (67 y.o. man). Circulatory changes in these three patients were treated by increasing the inspired sevoflurane concentration. We, however, speculate that the increase in inspired sevoflurane decreased the cardiac output and that the resulting increase in pulmonary wedge and capillary pressures was caused by an abrupt increase of arterial blood pressure, followed by a rapid increase in afterload due to cardiac suppression from the high concentration of sevoflurane. In 2 patients (74 y.o. man, 61 y.o. woman) arterial hypertension occurred during endotracheal extubation after sevoflurane anesthesia. Because of fast uptake and elimination of sevoflurane due to a low blood/gas partition coefficient, a fast awakening in the latter 2 patients, may be responsible for the abrupt increase in arterial blood pressure. In conclusion, it should be noted that pulmonary edema may be involved when severe circulatory changes occur in a patient undergoing sevoflurane anesthesia.
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PMID:[Acute pulmonary edema in five patients undergoing sevoflurane anesthesia]. 149 91

In 1989, corn screenings were associated with acute interstitial pulmonary edema, hydrothorax, and death in swine. Attack rate was 5-50%, case fatality rate was 50-90%, and clinical course was 1-2 days. Screenings from farms with pigs affected with pulmonary edema contained 20-330 micrograms fumonisin B1 per gram. Screenings containing 92 micrograms fumonisin B1 per gram fed to weanling pigs caused pulmonary edema and death. Sterilized corn inoculated with Fusarium moniliforme and diluted 1:1 with clean corn contained fumonisin B1 (17 micrograms/g) and caused acute pulmonary edema when fed for 5 days. Survivors developed subacute hepatotoxicosis with individual hepatocellular necrosis, hepatomegalocytosis, and increased numbers of mitotic figures. Similar liver lesions occurred in pigs given fumonisin B1 intravenously at 0.8 mg/kg body weight for 14 days.
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PMID:Characterization of an epizootic of pulmonary edema in swine associated with fumonisin in corn screenings. 155 70

Congestive heart failure (CHF) is typically associated with impaired left ventricular (LV) systolic performance. Few reports exist describing the long-term outcome in patients with CHF and normal LV systolic function. Fifty-two patients initially hospitalized with CHF and intact LV function (ejection fraction greater than or equal to 45%) were followed for 7 years. Mean age when initially identified was 71 +/- 11 years (range 36 to 96), and average LV ejection fraction was 61 +/- 11%. CHF was graded by a clinicoradiographic index, with a mean of 7.0 +/- 2.3 (range 3 to 12, 13 indicates worst CHF). A third heart sound was present in 19 patients (37%), and 17 (33%) had presented with acute pulmonary edema. Principal cardiovascular diagnoses were coronary artery disease in 27 (52%), hypertensive heart disease in 16 (31%) and restrictive cardiomyopathy in 7 (13%). At 7 years, cardiovascular mortality was 46% (24 of 52), and noncardiovascular mortality was 10% (5 of 52). Survival was not correlated with age, principal diagnosis, third heart sound, pulmonary edema at presentation, LV ejection fraction, or presence or degree of LV diastolic dysfunction. Cardiovascular morbidity, consisting of nonfatal recurrent CHF, myocardial infarction, unstable angina or other cardiovascular events occurred in 29% (15 of 52). Combined cardiovascular mortality and morbidity was 75% (39 of 52). In patients with CHF, intact LV systolic function does not confer the same favorable prognosis it defines in other clinical situations. For such patients, the risk of future cardiovascular events is high, a finding that should be considered when designing therapeutic strategies in this group.
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PMID:Long-term outcome in patients with congestive heart failure and intact systolic left ventricular performance. 157 93

The frequency, clinical characteristics, and outcome of patients admitted with heart failure to a district general hospital in North-West London serving a population of approximately 155,000 was assessed over a six-month period. The number of patients with heart failure was determined by both a prospective ward survey and a retrospective study of all patient records with diagnostic codes for heart failure or pulmonary oedema. During those six months, 2,877 patients were admitted to the medical and geriatric services of whom 140 (4.9%) had heart failure. Only 29 patients in heart failure were under the age of 65 years. In 86 patients the mode of presentation was acute pulmonary oedema. Fifty-two (37%) patients had an arrhythmia at the time of admission of whom 48 had atrial fibrillation. An electrocardiogram, a chest X-ray, and an echocardiogram were performed in 137, 136, and 81 patients respectively. The aetiology of heart failure was considered to be coronary artery disease (41%), valve disease (9%), hypertension (6%), cor pulmonale (4%), a dilated cardiomyopathy (1%), congenital heart disease (1%), thyrotoxicosis (1%), and unknown (36%). During the period of hospital stay 42 patients (30%) died; a further 20 patients (14%) died in a one-year follow-up. In a district general hospital heart failure is a common reason for admission and patients remain in hospital for a considerable time. Arrhythmias are commonly associated with heart failure. The prognosis is poor and the hospital mortality high. The management of heart failure is an important consideration in allocating hospital resources in a district general hospital.
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PMID:Heart failure in a district general hospital. 842 54

Low-molecular weight dextran is commonly used to prevent thrombosis after microvascular procedures; however, the potential complications of this drug are not well known. We report a case of acute pulmonary edema in a healthy person after elective microsurgery for treatment of a malignant tumor of the forearm. The mechanism of action of dextran and the pathophysiology of two potential adverse reactions to this drug are discussed. It is thought that in this patient pulmonary edema was caused by dextran toxicity.
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PMID:Acute pulmonary edema associated with use of low-molecular weight dextran for prevention of microvascular thrombosis. 170 97

Experiments in 150 albino rats have revealed that hyperbaric oxygenation (303.98 kPa) causes no decrease in pulmonary tissue hyperhydration and its blood filling induced by pituitrin administration. Hyperbaric oxygen therapy enhances pulmonary tissue peroxidation of lipids, without modifying them in blood. Application of lipid peroxidation inhibitors to prevention of pulmonary edema fails to affect pulmonary hydration and blood filling, which does not rule out the possibility of using them as protective agents against the toxic effects of oxygen in myocardial infarction which may be complicated by acute pulmonary edema.
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PMID:[Lipid peroxidation in vasopressin-induced pulmonary edema and hyperbaric oxygenation therapy]. 171 11

Scorpion sting in children is a hazardous and potentially fatal condition. Of 34 children admitted to hospital in Mahad, Maharashtra State, India following scorpion sting, 14 had hypertension (130/90-170/130 mmHg), five had myocardial failure, acute pulmonary oedema developed in nine, two had tachycardia (110-200/min) and four died. Analysis of data suggests that cardiovascular morbidity and mortality depend upon the time lapse between sting and administration of vasodilators. Current management of human scorpionism consists of early admission to hospital and immediate reduction of raised blood pressure with sublingual nifedipine while peripheral action of venom is antagonized by the post-synaptic alpha blocker prazosin; in addition, digoxin, frusemide, aminophylline and oxygen are administered. The patient is kept under close surveillance in an intensive care unit. Massive life-threatening pulmonary oedema is treated with a sodium nitroprusside drip. We suggest that aggressive medical management directed at the organ system specifically affected by scorpion venom can be effective.
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PMID:Cardiovascular manifestations of severe scorpion sting in India (review of 34 children). 172 99

Three schizophrenic adults with previous histories of using phenothiazine derivatives developed acute pulmonary edema after taking large amounts of these drugs. The clinical manifestations included coma (three), hypothermia (two), tachycardia (two), miosis (two) and hypotension (one). All three patients underwent gastric lavage and were treated supportively. The fulminant pulmonary edema in the three cases resolved within 18 to 40 h. The etiology of pulmonary edema following overdosage of phenothiazines remains unknown. The authors hypothesize that the most likely pathogenesis is a drug-induced neurogenic pulmonary edema resulting from a disturbance of hypothalamic function.
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PMID:Acute pulmonary edema induced by overdosage of phenothiazines. 172 53


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