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)

Ten patients, who were admitted to the Intensive Coronary Care Unit during a one year period with symptomatic bradycardia while on combination therapy with oral diltiazem and beta-blocker agents, are described. The important features of this adverse reaction to drug combination were that it appeared mainly in a relatively elderly age group and with presenting symptoms of lethargy, dizziness, syncope, chest pain, and (in one patient with poor left ventricular function) pulmonary edema. It was not dose dependent and occurred even in very low doses of each drug. Electrophysiologic abnormalities were localized to the sinus node in all 10 patients and the primary rhythm disorders were junctional escape rhythm, sinus bradycardia, and sinus pause. These rhythm abnormalities resolved within 24 h following withdrawal of the offending drugs. Temporary pacemaker insertion was necessary in four patients. The duration of drug combination used before the acute episode range from within hours to up to 2 years. In conclusion, although combination diltiazem/beta blocker therapy is very effective in ischemic syndrome, caution is advised when this combination is used especially in the elderly or in patients with left ventricular dysfunction or antecedent sinoatrial or atrioventricular conduction abnormality.
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PMID:Symptomatic bradycardia induced by the combination of oral diltiazem and beta blockers. 168 24

Male and female 16 to 18 month old C3Hf/Bd mice in a dermal carcinogenicity study were moribund or died at earlier time points than the expected 24 to 30 months. Clinical signs observed in both treated and control animals included dyspnea, lethargy, and death. Lesions seen in treated as well as control mice were cardiomegaly with myocardial degeneration and necrosis, hydrothorax and pulmonary edema, and ascites and chronic passive congestion of the liver. Mice were negative for serologic, bacteriologic and microscopic evidence of viruses, bacteria and protozoa which can induce heart lesions. Possible causes of the cardiomyopathy include metabolic, degenerative, genetic or undetermined infectious disease.
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PMID:Idiopathic cardiomyopathy in C3Hf/Bd mice. 270 3

Nine children, hospitalized for severe respiratory failure following scorpion envenomation, were a part of a group of 61 youngsters and infants admitted to the Pediatric Intensive Care Unit of the Soroka Medical Center, Beer-Sheva during the years 1983-87 because of scorpion venom intoxication. Four out of the nine had cardiogenic shock, three had severe systemic hypertension and one had severe airway obstruction. All nine patients had central nervous system manifestations, including lethargy, confusion and agitation (three cases), and markedly reduced level of consciousness (six cases). Hemodynamic studies performed in two patients showed 'high pressure' (cardiogenic) pulmonary edema. Seven patients recovered completely, one died and another one was left severely handicapped. Hydralazine i.v. showed a remarkable effect on the systemic blood pressure and central nervous system disturbances in addition to mechanical ventilation. Based on our own experience and previous clinical and experimental studies, the possible pathogenetic mechanisms underlying the respiratory and central nervous system dysfunction following scorpion sting are discussed.
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PMID:Respiratory failure in children following envenomation by the scorpion Leiurus quinquestriatus: hemodynamic and neurological aspects. 320 82

Five cases of coagulopathy caused by consumption of indanedione (diphacinone)-based rodenticides are reported. In each case, acute onset of lethargy and respiratory distress were the predominant initial clinical signs. Thoracic radiography revealed pulmonary edema, pleural effusion, and/or pericardial effusion as consistent findings. Laboratory evaluations confirmed coagulopathies that responded to vitamin K1 therapy.
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PMID:Diphacinone-induced coagulopathy in the dog. 394 17

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
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PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Eighty-seven cats with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of mitoxantrone, a dihydroxyquinone derivative of anthracene, which was administered at 21-day intervals at dosages ranging from 2.5 to 6.5 mg/m2 of body surface, IV. Eleven of these cats were treated concurrently with radiation but were evaluated separately. Each cat was evaluated for signs of toxicosis for 3 weeks after each dose was administered or until the cat developed progressive disease, or until the cat's quality of life diminished to an unacceptable level as determined by the owner or attending veterinarian. Although the primary purpose of this study was to determine a clinically useful dosage and to characterize the toxicoses associated with mitoxantrone administration, each cat was monitored for response to treatment. Forty-nine cats had been refractory to 1 or more treatment modalities prior to inclusion in this study. The most common signs of toxicosis after treatment with mitoxantrone were vomiting, anorexia, diarrhea, lethargy, sepsis secondary to myelosuppression, and seizures. Two cats died of complications that may have been attributed to mitoxantrone: 1 of cardiomyopathy and the other of pulmonary edema of an undetermined cause. Older cats were more likely to develop signs of toxicosis after the third or fourth mitoxantrone treatment than younger cats (P < or = 0.05). Cats with signs of toxicosis during the 21-day interval after administration of the first dose of mitoxantrone were significantly (P < or = 0.05) more likely to develop signs of toxicosis during the 21-day interval between the second and third doses of mitoxantrone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Toxicoses and efficacy associated with administration of mitoxantrone to cats with malignant tumors. 832 Jan 52

Since mid-1989, 37 cases of oleander poisoning in livestock have been diagnosed at the California Veterinary Diagnostic Laboratory System. The most frequent source for oleander exposure was plant clippings. Sudden death was the most common presenting complaint. Other signs reported included diarrhea, pulmonary edema, tachycardia, cardiac arrhythmias, colic, and lethargy. In the past, a presumptive diagnosis of oleander poisoning could be based only on matching clinical signs with evidence of consumption of oleander. A new 2 dimensional Thin-layer chromatography analysis of ingesta for oleandrin and an awareness of lesions in heart muscle have greatly improved the ability to diagnose oleander toxicosis.
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PMID:Diagnosis of oleander poisoning in livestock. 884 81

Fischer 344 rats (250-300 g) were exposed to the resulting aerosols from the pyrolysis of Spectrex Fire Extinguishant (SFE) Formulation A, a pyrotechnically generated aerosol fire suppressant, at a loading equivalent of 50 or 80 g m(-3) air for 15 or 60 min. Exposures were conducted in a 700-1 whole-body inhalation chamber under static conditions. The chamber atmosphere was analyzed for mass aerosol concentration and size distribution. Clinical observations were taken throughout the exposure. Animals were euthanized at 1 h, 6 h, 24 h, 7 days or 14 days post-exposure and underwent histopathological examination, enzyme analyses and wet/dry lung weight determination. No deaths occurred during the study. Animals exhibited signs of dyspnea, coughing, lack of coordination and lethargy during each exposure. These signs became more pronounced as the load and exposure length increased. No lesions were noted in the trachea, lung, heart or abdominal organs upon gross examination. A reversible pulmonary edema and olfactory necrosis were observed only in those animals exposed to an SFE loading equivalent to 80 g m(-3) for 60 min. Protein concentrations increased in the bronchoalveolar lavage but no changes in enzyme levels were observed. There was no significant difference between the control groups and the exposure groups for wet/dry lung weight determination.
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PMID:Evaluation of the respiratory tract after acute exposure to a pyrotechnically generated aerosol fire suppressant. 918 52

From 1994 to 1999, 16 captive African hedgehogs (Atelerix albiventris), from among 42 necropsy cases, were diagnosed with cardiomyopathy. The incidence of cardiomyopathy in this study population was 38%. Fourteen of 16 hedgehogs with cardiomyopathy were males and all hedgehogs were adult (>1 year old). Nine hedgehogs exhibited 1 or more of the following clinical signs before death: heart murmur, lethargy, icterus, moist rales, anorexia, dyspnea, dehydration, and weight loss. The remaining 7 hedgehogs died without premonitory clinical signs. Gross findings were cardiomegaly (6 cases), hepatomegaly (5 cases), pulmonary edema (5 cases), pulmonary congestion (4 cases), hydrothorax (3 cases), pulmonary infarct (1 case), renal infarcts (1 case), ascites (1 case), and 5 cases showed no changes. Histologic lesions were found mainly within the left ventricular myocardium and consisted primarily of myodegeneration, myonecrosis, atrophy, hypertrophy, and disarray of myofibers. All hedgehogs with cardiomyopathy had myocardial fibrosis, myocardial edema, or both. Other common histopathologic findings were acute and chronic passive congestion of the lungs, acute passive congestion of the liver, renal tubular necrosis, vascular thrombosis, splenic extramedullary hematopoiesis, and hepatic lipidosis. This is the first report of cardiomyopathy in African hedgehogs.
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PMID:Cardiomyopathy in captive African hedgehogs (Atelerix albiventris). 1102 39


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