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

Heart and lung transplantation has only provided long-term survival for patients with end-stage cardiopulmonary disease. Many more patients of potential recipients cannot receive the transplantation because of a pause of satisfactory donors. One of its reason is difficulty in prolonged heart-lung preservation and this has imposed a significant barrier to donor procurement. Using Autoperfusion of heart and lung, six hours preservation was successfully achieved in six mongrel dogs and an adequate condition for preservation was evaluated. 1. Glucose metabolism, 2. Electrolytes, 3. Acid-base balance, 4. Pulmonary blood flow, 5. Temperature, 6. Ventilation were considered important factors for long hours preservation. Heart and lung preserved for six hours were transplanted in thirteen dogs in heterotopic and orthotopic models and their functions were evaluated two hours after transplantation. The cardiac function was well preserved and pathological changes in cardiac muscle were minimum. But lung preservation was not so stable. Levels of PaO2 were variable and pathological changes of the donor lungs such as pulmonary edema, emphysema, etc were observed. Further studies were needed for lung preservation.
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PMID:[An experimental study on the heart and lung preservation and transplantation. Autoperfusion method and cardiac and pulmonary functions after transplantation]. 314 58

The clinical signs and lesions of Nubian goats and Desert sheep orally dosed with fresh and dry leaves and stems of Ipomoea carnea at 2.5, 5 and 10 g/kg/day were studied. The signs of Ipomoea poisoning were inappetence, depression, weakness of the hind limbs, dyspnea, staggering, and pallor of the visible mucous membranes. The main lesions were focal necrosis and fatty vacuolation of centrilobular hepatocytes, accumulation of fibroblasts in hepatic portal tracts, degeneration or necrosis of the cells of the renal proximal convoluted tubules, hemorrhage in renal cortices, in renal medullas and in cardiac muscle fibers, focal pulmonary edema, and emphysema and straw-colored fluid in serous cavities. Increased serum aspartate amino transferase and ammonia concentrations, and decreased concentrations of total protein, calcium and magnesium in the serum of Ipomoea-poisoned animals were detected. Hematological changes indicated the development of normocytic normochromic anaemia.
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PMID:The effects of Ipomoea carnea on goats and sheep. 362 12

The Gaboon viper has acquired an impressive reputation which is at least partly unfounded. This handsome animal with such striking features is undoubtedly docile which accounts for the very low incidence of bite amongst humans. There are only six detailed clinical reports on the effect of bite and these are summarized in the review. The viper does indeed produce prodigious amounts of venom, but the toxicity, weight for weight, is rather low compared to other poisonous snakes. Venom extractions have been carried out on four snakes over a 13-year-period and the effects of this venom have been studied in a variety of experimental animals. Systemic envenomation is characterized by immediate abrupt hypotension, subsequent cardiac damage and dyspnoea. The individual venom components responsible for these effects have not been isolated but it seems likely that the two enzymes which have been studied extensively (phospholipase A2 and the thrombin-like enzyme, gabonase) do not contribute significantly to lethality. We propose three principal activities which give rise to the major signs of systemic envenomation. Haemorrhagin; causing widespread damage to microvasculature which leads to the pulmonary oedema and hence dyspnoea, and locally causes blistering. Cardiotoxin; a long-acting material causing cardiac muscle damage, arrhythmia and ultimately cardiac failure. Peripheral vasodilator; a short acting effect, operating either locally via bradykinin formation and/or unknown peptides or centrally on the vasomotor centre.
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PMID:The Gaboon viper (Bitis gabonica): its biology, venom components and toxinology. 639 43

Feline and canine cardiomyopathies (primary myocardial diseases) were reviewed and divided into three groups based on the clinical, hemodynamic, angiocardiographic, and pathologic findings: (1) feline and canine hypertrophic cardiomyopathy, (2) feline and canine congestive (dilated) cardiomyopathy, and (3) feline restrictive cardiomyopathy. All three groups consisted predominantly of mature adult male cats and dogs. Cardiomyopathy in the hamster and turkey was also reviewed. The most common presenting signs were dyspnea and/or thromboembolism in the cat, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (groups 1 and 3) or without (group 2) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end-diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (group 1), left ventricular dilatation (group 2), or midventricular stenosis (group 3). Some cats in groups 1 and 3 also had evidence of left ventricular outflow obstruction. The principal pathologic findings in all of the cats and dogs were left atrial dilation, hypertrophy, increased septal:left ventricular free wall thickness ratio with disorganization of cardiac muscle cells (group 1); dilatation of the four chambers with degeneration of cardiac muscle cells (group 2); and extensive endocardial fibrosis and adhesion of the left ventricle (group 3). Aortic thromboembolism was commonly observed in the cats of all three groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat or dog is similar to the three forms of cardiomyopathy in humans (hypertrophic, congestive, and restrictive).
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PMID:Animal models of primary myocardial diseases. 644 12

In a 21/2-year period, hypertrophic cardiomyopathy was found at necropsy of 23 cats that died (13 cats) or were euthanatized (10) because of problems associated with hyperthyroidism. Of these, 4 (17%) also had evidence of cardiac failure (pulmonary edema or pleural effusion). The mean body weight of the cats with hyperthyroidism and hypertrophic cardiomyopathy was significantly less (P less than 0.001) than that of clinically normal cats and cats with primary cardiomyopathy (congestive or restrictive) or excessive moderator band cardiomyopathy. In addition, the ratio of heart weight to body weight was significantly greater (P less than 0.001) in the 23 hyperthyroid cats than in the normal cats and cats with primary cardiomyopathy. Twenty (87%) of the cats had symmetric hypertrophy of the ventricular septum and left ventricular free wall, whereas the remaining 3 cats had disproportionate thickening of the ventricular septum, compared with the free wall, similar to what is found in cats with asymmetric hypertrophic cardiomyopathy. Histologic cardiac abnormalities included large, hyperchromatic nuclei, interstitial fibrosis, endocardial fibroplasia, fibrosis of the atrioventricular node, and marked disorganization of cardiac muscle cells. The study showed that hypertrophic cardiomyopathy develops in most hyperthyroid cats, some of which also develop congestive heart failure. Although the signs of heart disease in primary myocardial disease and thyrotoxic disease are similar, the characteristic signalment and clinical signs of hyperthyroidism should lead one to suspect the association of hypertrophic cardiomyopathy with the hyperthyroidism.
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PMID:Hypertropic cardiomyopathy and hyperthyroidism in the cat. 654 Feb 56

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

Seven related Quarter Horse foals that died by 7 weeks of age were examined for glycogen branching enzyme (GBE) deficiency. Clinical signs varied from stillbirth, transient flexural limb deformities, seizures, and respiratory or cardiac failure to persistent recumbency. Leukopenia (5 of 5 foals) as well as high serum creatine kinase (CK; 5 of 5), aspartate transaminase (AST; 4 of 4), and gamma glutamyl transferase (GGT; 5 of 5) activities were present in most foals, and intermittent hypoglycemia was present in 2 foals. Gross postmortem lesions were minor, except for pulmonary edema in 2 foals. Muscle, heart, or liver samples from the foals contained abnormal periodic acid Schiff's (PAS)-positive globular or crystalline intracellular inclusions in amounts proportional to the foal's age at death. Accumulation of an unbranched polysaccharide in tissues was suggested by a shift in the iodine absorption spectra of polysaccharide isolated from the liver and muscle of affected foals. Skeletal muscle total polysaccharide concentrations were reduced by 30%, but liver and cardiac muscle glycogen concentrations were normal. Several glycolytic enzyme activities were normal, whereas GBE activity was virtually absent in cardiac and skeletal muscle, as well as in liver and peripheral blood cells of affected foals. GBE activities in peripheral blood cells of dams of affected foals and several of their half-siblings or full siblings were approximately 50% of controls. GBE protein in liver determined by Western blot was markedly reduced to absent in affected foals, and in a half-sibling of an affected foal, it was approximately one-half the amount of normal controls. Pedigree analysis also supported an autosomal recessive mode of inheritance. The affected foals have at least 2,600 half-siblings. Consequently, GBE deficiency may be a common cause of neonatal mortality in Quarter Horses that is obscured by the variety of clinical signs that resemble other equine neonatal diseases.
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PMID:Glycogen branching enzyme deficiency in quarter horse foals. 1181 63

Here, we aimed to determine the toxicity of Cryptostegia venusta in goats and rats. We orally administered a single 60 g dose of shredded C. venusta leaves per kilogram of body weight to three goats. The animals were necropsied after death, and tissue sections were collected and routinely processed for histopathological analyses. Additionally, we separated 25 adult male Wistar rats (each weighing about 150 g) into five groups: an untreated control group and groups orally treated with 1, 3, 10, or 60 g/kg doses. Rats were sacrificed 72 h after administration of the C. venusta extract, and tissue sections collected for histopathological analyses. All goats presented signs of apathy, salivation, frequent urination, and eventually fatigue 4-6h after receiving C. venusta. Two goats died 20 h after administration, and the third was sacrificed in extremis. The only histopathological finding observed in the goats was lung edema. No rats died during the experimental period or presented any clinical signs or macroscopic lesions. However, both goats and rats exhibited degeneration and multifocal necrosis of cardiac muscle fibers. From our results, we conclude that the C. venusta plant is capable of promoting cardiotoxicity.
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PMID:Pathological effects of Cryptostegia venusta toxicity in goats and rats. 2067 85

Heart failure, a common condition affecting older patients, is associated with increased hospitalization and mortality rates among geriatric patients. We describe the case of an 86-year-old woman with moderate renal failure, who presented pulmonary edema and severe myocardial dysfunction due to hypocalcemia. Renal failure, but also the combination of additional factors, may have contributed to hypocalcemia, including vitamin D deficiency, loop diuretics and glucocorticoid therapy - which alone can give rise to sodium retention and calciuresis, and worsens hypocalcemia. Although in animal experiments hypocalcemia has been shown to lead to cardiac decompensation, heart failure from hypocalcemia is quite rare in clinical practice. Calcium plays a key role in cardiac muscle contraction and metabolism. It is recommended that physicians check serum calcium levels in the elderly, as hypocalcemia is a reversible cause of heart failure.
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PMID:Hypocalcemia: a sometimes overlooked cause of heart failure in the elderly. 2323 16

This investigation detailed the clinical disease, gross and histologic lesions in juvenile openbill storks (Anastomus oscitans) intranasally inoculated with an avian influenza virus, A/chicken/Thailand/vsmu-3 (H5N1), which is highly pathogenic for chickens. High morbidity and mortality were observed in openbill storks inoculated with HPAI H5N1 virus. Gross lesions from infected birds were congestion and brain hemorrhage (10/20), pericardial effusions, pericarditis and focal necrosis of the cardiac muscle (2/20), pulmonary edema and pulmonary necrosis, serosanguineous fluid in the bronchis (16/20), liver congestion (6/20), bursitis (5/20), subcutaneous hemorrhages (2/20) and pinpoint proventiculus hemorrhage (2/20). Real time RT-PCR demonstrated the presence of viral RNA in organs associated with the lesions: brain, trachea, lungs, liver, spleen and intestines. Similar to viral genome detection, virus was also isolated from these vital organs. Antibodies to influenza virus detected with a hemagglutination inhibition test, were found only in the openbill storks who died 8 days post-inoculation.
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PMID:Susceptibility of openbill storks (Anastomius oscitans) to highly pathogenic avian influenza virus subtype H5N1. 2443 15


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