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)

Fifty-two cases of acute phase subarachnoid hemorrhage were studied by brain CT scanning to determine the presence and incidence of ischemic myocardial disorder, the relationship between ischemic change and severity, disease prognosis, and the relationship between acute phase circulatory dynamics and so-called neurogenic pulmonary edema. In all cases, ECGs were carried out and CPK-MB determined. Some of the patients underwent Tl myocardial scintigraphy, echocardiography, cardiac catheterization, as well as circulatory dynamic investigation (by Swan-Ganz catheter) and arterial blood gas analysis. In 31 of the 52 cases (59.6%), 3-day ECG series revealed ischemic changes. These findings were backed up by other cardiac function tests, thus suggesting that myocardial ischemia was present. Results in cases undergoing cardiac catheterization revealed that the myocardial ischemic changes were not due to organic constriction of the coronary artery. Included in those cases in which ECG markedly changed and CPK-MB rose substantially were many patients for whom the prognosis was poor. Evaluation of respiratory function and circulatory dynamics in cases of so-called neurogenic pulmonary edema seemed to indicate decline in cardiac function owing to myocardial ischemic change. This could account for onset of symptoms. These findings support the need for adequate circulatory management in cases of acute subarachnoid hemorrhage with pulmonary edema and/or changes on ECG. In such cases, concurrent catheterization and cerebral angiography (cerebro-cardiac catheterization: CCC) proved effective for evaluating cardiac function and determining whether heart disease was also present.
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PMID:[Ischemic myocardial disorder in acute phase subarachnoid hemorrhage: clinical study of 52 patients]. 204 49

Thiourea (TU), a very effective hydroxyl radical (.OH) scavenger, has little value as a probe of .OH in vivo because it causes fatal pulmonary edema. To test the hypothesis that TU-induced lung injury results from .OH-mediated oxidation of TU to toxic cyanamide, we pretreated rats with .OH scavengers, dimethylsulfoxide (DMSO), ethanol, and mannitol, prior to treatment with TU (3 mg/kg), preventing 91, 63, and 53%, respectively, of increases in lung weight to body weight ratios and 93, 67, and 46% of increases in lung lavage albumin concentrations. Furthermore, treatment of rats with cyanamide (CYN) (100 mg/kg) also caused increases in lung weight to body weight ratios (CYN: 7.39 +/- 0.57 X 10(-3) vs. controls: 5.46 +/- 0.26). N,N'-dimethylation of TU (DMTU) prevented TU toxicity, because treatment with DMTU did not significantly increase lung weight to body weight ratios (DMTU: 5.12 +/- 0.16 X 10(-3) vs. controls: 5.46 +/- 0.26) or lung lavage albumin (DMTU: 14 +/- 1 mg/100 ml vs. controls: 11 +/- 1). DMTU remained a very effective in vivo .OH scavenger, increasing survival of lethally irradiated mice treated with 600 mg/kg DMTU to 79% compared with 8% in untreated controls.
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PMID:Prevention of thiourea-induced pulmonary edema by hydroxyl-radical scavengers. 641 79

A 34-year-old housewife with alcohol dependence vomited severely, lost consciousness, and died after she took more than 20 ml of 1% calcium cyanamide, and alcoholic beverage containing about 129 g of ethyl alcohol. An autopsy was performed around 16 h after death. The body weighed 55.5 kg, and moderate lung edema was found. Ethanol concentrations were 4.24 mg/g in the left heart blood, 4.39 mg/g in the right heart blood, and 21.55 mg/g in the stomach contents. Cyanamide concentrations were 0.63 microgram/g in the left heart blood, 0.20 microgram/g in the right heart blood, and 0.22 microgram/g in the stomach contents. The cause of death was determined to be acute ethanol intoxication with alcohol-cyanamide reaction.
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PMID:A fatal case of drinking and cyanamide intake. 918 22