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)

Oral administration of Galega officinalis L to sheep demonstrated a marked variation in individual animal susceptibility to the toxic effects of the plant. As little as 5 g/kg of dried ground plant induced moderate tracheal frothing in 1 ewe while nearly 5 times that amount failed to elicit any recognizable toxic effects such as frothing, pulmonary edema or hydrothorax in others. Ten g/kg induced severe effects in 3 ewes. Ewes administered levels of plant between 5 and 24 g/kg had toxic effects whose severity was often unrelated to level administered. There was no apparent difference in average severity of clinical signs of toxicity nor pathologic lesions to challenge doses of 24 g/kg of the plant between groups of ewes with an immediate previous history of increasing doses of the plant and others with no history of ingesting the plant. Previously reported apparent induced adaptation or tolerance to G officinalis L in some animals is more likely to have been a result of the extreme variation in individual animals susceptibility.
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PMID:Individual animal susceptibility and its relationship to induced adaptation or tolerance in sheep to Galega officinalis L. 318 60

The gross and histopathological lesions of 10 cases in a natural outbreak of aflatoxicosis amongst dogs in the Republic of South Africa are reported. The 10 cases were classified as acute (1 case), subacute (7 cases) and chronic (2 cases) on the basis of the nature, degree and extent of the following histopathological fractures: hepatocellular fatty degeneration, necrosis or regeneration; proliferation of bile ductules; accumulation of bile within the canaliculi; fibroplasia; and, mucoid degeneration, necrosis or segmental atrophy of the larger intrahepatic bile ducts. Fatty degeneration was noted grossly in the livers of all 10 cases and bile stasis in 4. Varying degrees of fibrosis were present depending on the stage of the disease. In the 2 chronic cases in which nodular regeneration was also observed fibrosis was pronounced. Other macroscopic findings included icterus, anaemia, ascites, hydrothorax, hydropericardium, anasarca, pulmonary oedema, gastro-enterorrhagia and nephrosis.
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PMID:Pathological findings in a natural outbreak of aflatoxicosis in dogs. 344 19

Cisplatin (cis-diamminedichloroplatinum; Platinol, Bristol, Syracuse, NY) was administered to 11 cats, divided into three groups of experimental and clinical patients. In group 1, cisplatin was administered at a dose of 60 mg/m2 to four cats. In an attempt to avoid renal toxicity, saline diuresis was induced by administering 0.9% saline solution intravenously at a rate of 20 ml/kg/hr for 4 hours before and 2 hours after cisplatin administration. All four cats became dyspneic and died 48-96 hours after cisplatin administration. Postmortem findings included severe hydrothorax, pulmonary edema, and mediastinal edema. In group 2, four experimental cats entered a trial comparing the effects of saline diuresis and cisplatin (60 mg/m2) with the effects of saline diuresis and placebo (0.9% saline solution). The cats in the saline control group remained completely normal, while the cats that received cisplatin developed clinical signs and gross postmortem pulmonary changes identical to those in the first group of cats. Histopathologic examination showed that the alveolar septa were thickened and congested, and contained macrophages, occasional neutrophils, thrombi, and small foci of necrosis and fibrin. Microangiopathic changes were seen in the alveolar capillaries. In the third group, three additional cats were treated with a lower dose of cisplatin. Two cats that received 40 mg/m2 of cisplatin developed pulmonary changes similar to, but less severe than, those seen in the cats that received the higher dose of cisplatin. One cat treated with 20 mg/m2 of cisplatin showed no pulmonary changes ante mortem or post mortem. This series of 11 clinical and experimental cases identifies an apparent species-specific, dose-related, primary pulmonary toxicity of cisplatin in cats.
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PMID:Cisplatin toxicity in cats. 350 19

N-Methylthiobenzamide (NMTB) produces pulmonary edema, hydrothorax, and death in rodents. The objectives of the present studies were to establish a relationship between the lethality of NMTB and its pneumotoxicity and to explore the role of S-oxidation in these events. Pulmonary injury was assessed by measuring [14C]thymidine incorporation into pulmonary DNA. Administration of NMTB resulted in increased pulmonary [14C]thymidine incorporation in both rats and mice. These increases were blocked in both species by pretreatment of animals with sublethal doses of NMTB. However, the lethality of NMTB was not blocked in mice by prior administration of NMTB even though this procedure has been shown to protect rats. 1-Methyl-1-phenyl-3-benzoylthiourea (MPBTU) protected both rats and mice from lethal doses of NMTB and blocked NMTB-induced increases in pulmonary [14C]thymidine incorporation. N-Methylthiobenzamide S-oxide (NMTBSO), a metabolite of NMTB, produced lung injury which was similar to that produced by NMTB. NMTBSO was more potent than NMTB when administered iv, but not when given ip. The role of hepatic metabolism in NMTB pneumotoxicity was examined by administering NMTB to rats which had either undergone partial hepatectomy or been pretreated with N-octylimidazole. Neither of these procedures diminished the lethality of NMTB. These data suggest that NMTB lethality is mediated by pulmonary injury resulting from NMTB S-oxidation in the lung.
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PMID:The role of metabolism in N-methylthiobenzamide-induced pneumotoxicity. 393 Dec 98

Suspected monensin toxicosis was seen in feedlot cattle aged 6 to 9 months. Twenty cattle died following inclusion of monensin in the feed at 400g/tonne, which was 13 times the recommended level. The deaths occurred over 2 weeks. Clinical signs were inappetance, respiratory distress and sudden death. Post-mortem features were those of right-sided heart failure and included dependent subcutaneous oedema, ascites, hydrothorax, and periancinar hepatocyte congestion and necrosis. However, in contrast to previous reports no myocardial necrosis was found, but focal skeletal muscle necrosis was observed. Additional findings were marked pulmonary oedema accompanied by fibrin and erythrocyte exudation into alveoli and interlobular lymphatics. From these findings it appears that monensin, as well as affecting both cardiac and skeletal muscle, has a primary effect on lung vasculature.
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PMID:Suspected monensin toxicosis in feedlot cattle. 402 19

Of 1,994 yearling and 2-year-old cattle in a winter feeding program, 117 died within 42 days of being fed toxic amounts of monensin sodium in a liquid protein supplement. Death losses commenced on the third day after ingestion of a toxic amount in the feed. Clinical signs in cattle that died in less than 9 days included anorexia, pica, diarrhea, depression, mild hindlimb ataxia, and dyspnea. Gross necropsy findings in cattle dying in the acute phase of the illness included hydrothorax, ascites, and pulmonary edema, as well as petechial hemorrhages, edema, and yellow streaking in skeletal and cardiac muscle. Cattle dying after 9 days had gray streaks in heart and skeletal muscle, generalized ventral edema, enlarged, firm, bluish discolored liver, and enlarged heart. Microscopic changes in cattle dying in the acute phase (less than 9 days) consisted of pulmonary edema, congestion, and hemorrhage. Cardiac and skeletal muscle had localized areas of edema, hemorrhage, and coagulative necrosis. In cattle dying after 9 days of illness, the changes included lymphocytic infiltration, sarcolemmal nuclear proliferation, and fibrosis in skeletal and cardiac muscle. Lungs contained increased alveolar macrophages and a few neutrophils. Centrilobular necrosis and mild fibrosis were found in the liver. Changes varied somewhat according to the area of heart or skeletal muscle that was affected. Active muscles, eg, those in the heart ventricles and diaphragm, were altered most severely. Intoxication appeared to be a result of sedimentation of monensin in the molasses carrier to give remarkable concentrations of the substance at the bottom of the holding tank.
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PMID:Accidental monensin sodium intoxication of feedlot cattle. 673 46

Primary thiomides such as thiobenzamide (TB) are well known hepatotoxins in the rat. Among para-substituted TB derivatives relative hepatotoxicity varies in accordance with the electronic properties of the parasubstituent. In contrast, several N-substituted TBs have been found to be potent lung toxins in rats and mice. For N-methylthiobenzamide (NMTB) the LD50 was found to be 0.315 (95% confidence interval (CI) 0.228-0.436) mmol/kg in the rat and 0.224 (95% CI 0.191--0.264) mmol/kg in the mouse. The N-mono-substituted TBs produce alveolar and perivascular pulmonary edema, together with massive pleural effusions (hydrothorax). In this regard their toxicity resembles qualitatively that of the arylthioureas. Furthermore, pretreatment of rats with sub-lethal doses of NMTB was found to protect them against subsequent challenge with supra-lethal doses. N,N-Dimethylthiobenzamide (DMTB) also causes lung injury in the rat, but only at much higher doses than with the N-mono-substituted TBs. The similarity in toxic responses elicited by the N-mono-substituted TBs and the arylthioureas is paralleled by similarities in their chemical structures and their metabolic disposition which involves (among other things) S-oxygenation by the microsomal flavin-containing monooxygenase (EC 1.14.13.8). Thus, a possible role for S-oxidized metabolites in the lung toxicity of these compounds must be considered.
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PMID:Pneumotoxic effects of thiobenzamide derivatives. 708 87

The Epstein-Barr virus nuclear antigen-leader protein (EBNA-LP) is required for high efficiency B lymphocyte growth transformation by the virus. To test the potential contribution of EBNA-LP to tumorigenesis in vivo, we produced transgenic mice carrying an EBNA-LP cDNA construct, using the widely expressed metallothionein promoter. Expression of EBNA-LP was detected in liver, kidney, heart, lung and spleen. There were no apparent oncogenic consequences of EBNA-LP expression. Unexpectedly however, at ages ranging from about 4 months to over a year, transgenic mice developed symptoms of congestive heart failure, including left ventricular dilatation, right ventricular hypertrophy, left atrial thrombosis, pulmonary oedema and hydrothorax. Fibrillation was not apparent in the electrocardiograph; however a reduction in T-wave amplitude suggested that the development of an abnormality of ventricular repolarization may precede the manifestation of overt symptoms. The highly predictable development of dilated heart failure in these transgenic mice suggests they may be a useful model for the pathophysiological changes associated with human dilated cardiomyopathy.
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PMID:Dilated heart failure in transgenic mice expressing the Epstein-Barr virus nuclear antigen-leader protein. 839 79

From a series of experimental studies with pigs (12-16 kg), either pulmonary edema or liver failure emerged as a distinct pathogenetic expression of fumonisin B1 (FB1) toxicosis. The primary determinant as to which pathogenetic consequence developed was the quantity (dose) of the mycotoxin fed or intubated per kilogram of body weight per day. Pigs intubated with a minimum of 16 mg FB1/kg/day developed severe interlobular edema with or without hydrothorax and variably severe pulmonary edema. Pigs intubated with < 16 mg FB1/kg/day or pigs fed diets containing 200 mg FB1/kg of feed developed marked icterus and hepatocellular necrosis. The spectrum of degrees of severity of pulmonary edema observed in the experimental pigs allowed rational speculation regarding evolution of the pathologic changes.
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PMID:Fumonisin toxicosis in swine: clinical and pathologic findings. 850 2

Aflatoxin (AF)-contaminated and fumonisin B1 (FB1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of AF and 0 mg of FB1/kg of feed (control); 2.5 mg of AF/kg of feed; 100 mg of FB1/kg of feed; or 2.5 mg of AF plus 100 mg of FB1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by AF and AF plus FB1 diets. The FB1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum gamma-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The FB1-alone diet increased serum GGT activity, whereas the AF plus FB1 diet increased serum aspartate transaminase, cholinesterase, alkaline phosphatase, and GGT activities, increased RBC count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the AF plus FB1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the AF plus FB1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the FB1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the FB1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the AF plus FB1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The AF diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the AF-diet groups. Renal tubular nephrosis was observed in barrows of the FB1-diet group, but this was not consistent in the AF plus FB1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the AF and FB1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that AF and FB1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease.
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PMID:Influence of aflatoxin and fumonisin B1-containing culture material on growing barrows. 859 31


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