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

Ozone is a strong oxidizing agent that can cause lung damage and edema. There is evidence that it does so by causing peroxidation of membrane lipids. However, the elevation in lung activity of copper, zinc superoxide dismutase (Cu, ZnSOD), and manganese superoxide dismutase (MnSOD) during exposure to ozone suggests that increased production of superoxide could contribute to lung edema caused by ozone. This latter observation, and preliminary evidence that treatment of rats with endotoxin elevates lung activity of MnSOD without elevation of the activity of Cu, ZnSOD, catalase (CAT), or glutathione peroxidase (GP), led to the present study. We treated rats with endotoxin, exposed them to different concentrations of ozone, measured lung wet weight to dry weight ratio, thiobarbituric acid-reactive material (TBAR), and assayed lung tissue for Cu, ZnSOD, MnSOD, CAT, and GP activity. Our major findings are, (1) a strongly edemogenic concentration of ozone-lowered MnSOD activity; (2) endotoxin treatment of air-breathing rats did not decrease lipid peroxidation as indicated by the lung concentration of TBAR; (3) induction of increased MnSOD activity in lung by treatment with endotoxin was associated with virtually complete protection against an otherwise edemogenic concentration of ozone, with less lipid peroxidation, and with less loss of weight; and (4) this protection occurred without elevated Cu, ZnSOD, CAT, or GP activity.
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PMID:Endotoxin treatment protects rats against ozone-induced lung edema: with evidence for the role of manganese superoxide dismutase. 155 46

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

Cadmium is a highly toxic element that is cumulative and has a long biological half-life in mammals. The severe toxicity of cadmium in man has been known for more than 100 years. Despite the knowledge that cadmium is toxic, only 20 human cases of poisoning via ingestion were recorded prior to 1941, whereas in the ensuing five-year period more than 680 cases of cadmium poisonings from accidental oral ingestion of this metal were documented. Some of the recorded effects of exposure to cadmium in laboratory animals include renal tubular damage, placental and testicular necrosis, structural and functional liver damage, osteomalacia, testicular tumors, teratogenic malformations, anemia, hypertension, pulmonary edema, chronic pulmonary emphysema, and induced deficiencies of iron, copper, and zinc. Some of these effects have also been observed in human after accidental exposures to cadmium oxide fumes and are characteristic of the syndrome described in Japan as Itai Itai disease in which ingestion of cadmium is the inciting chemical.
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PMID:Cadmium inhalation and male reproductive toxicity. 240 89

The harmful effect of iron excess was studied in an experiment using fifteen adult sheep. The animals were divided into three groups of 5 each. The sheep of the group I were kept as controls, those of the group II and III were supplemented with iron in doses of 80 and 40 mg/kg body weight (BW)/24 h respectively. The animals of group II died after a period of 3-7 weeks showing anorexia, loss of weight, diarrhoea, depression and symptoms of circulatory and respiratory failure. From the animals of group III one died after 13 weeks, with symptoms of pulmonary oedema, while the other 4 survived for 22 weeks, together with the animals of the control group. The iron-supplemented animals presented increased values of Serum Iron (SI), Total Iron Binding Capacity (TIBC), percent Transferring Saturation (% SAT), Alanino aminotransferase (ALT), serum Alkalin Phosphatase (SAP), Serum Urea Nitrogen (SUN) Creatinine, Phosphorus and decreased values of serum Copper concentration. These parameters were greater in group II. The iron concentration in the liver, spleen, myocardium and kidneys was also much higher than in the controls. The histological examination revealed degeneration of the liver, spleen, myocardium and kidneys in both groups, while cells overloaded with hemosiderin were seen in the third group only. In conclusion, it was shown that chronic intoxication may occur in sheep overdosed with iron. The toxic dose of iron ranged between 40 and 80 (mg/Kg body weight) per day and was close to 40 mg, when iron was administered in the soluble from FeCl3.6H2O.
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PMID:Iron toxicity in sheep. 253 32

A case of fatal suicidal ingestion of "Super Blue (Gun Blue)" (gun-blueing) is presented. Post-mortem examination of the patient revealed pulmonary edema with pleural effusion and congestion of the kidney. Necrosis of proximal tubules was found in the kidney by histological examination. "Super Blue" contains 4% selenious acid and 2.5% cupric sulfate in HCl. Levels of selenium and copper in tissues of the toxic case and normal individuals were determined. The selenium levels of tissues of the patient were 9-90-fold higher than that of normal subjects, whereas concentrations of copper were about 2-fold compared to that of control levels. The highest levels of selenium in the tissues of the patient were found in the lung, kidney and stomach contents.
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PMID:An autopsy case of acute selenium (selenious acid) poisoning and selenium levels in human tissues. 374 7

Cases of fatal poisoning with cupric compounds are relatively rare in everyday life and are not covered much in forensic literature. A case was encountered of fatal poisoning with a blue vitriol solution introduced into the uterine cavity in order to interrupt a pregnancy. A 39-year-old woman brought to the hospital by ambulance complained of pain in the lumbar region and profuse bloody genital discharge, which had appeared 3 days earlier. She believed she was 2 months pregnant and denied artificial interruption of the pregnancy. Upon examination, her condition was grave: a weak pulse of 80; blood pressure 100/60. The abdomen was soft, the liver and spleen not enlarged. Pasternak symptom was negative. The uterus was soft, painless and enlarged to 9 weeks of pregnancy. The uterine cervix was clean, the orifice closed. Discharge was profuse and bloody. The diagnosis was that she was 9 weeks pregnant and had a missed criminal abortion. Scraping out the uterus and corresponding therapy to control bleeding were ineffective. An operation was performed--extirpation of the uterus. However, despite the steps taken, the bleeding did not stop, and the patient's condition continued to worsen. 10 hours after being admitted to the hospital, she died. During forensic investigation, diffused, violet-colored cadaverous spots were discovered. Extensive subcutaneous hemorrhage was detected around the areas of injection. The skin covering was edematous; when pressed with a finger, areas of depression remained. There was about 250 ml of watery blood in the abdominal cavity. Internal organs were anemic. There were multiple subpleural, subepicardial, subcapsular, intraorgan and intramuscular micro- and macro-punctate hemorrhages; bleeding into the mucosa of the gastrointestinal tract and urinary tracts; and cerebral and pulmonary edema. Forensic histological examination showed acute circulatory disturbance with perivascular and peridiapedetic hemorrhage; concentrations of aggregated and hemolyzed erythrocytes in the small vessels and capillaries; cerebral, pulmonary and stromatic edema. In the kidneys there was coaugmentation of renal glomeruli; epithelial necrosis of part of the coiled ducts; lower epithelium in places had pigment grains; primarily in openings of straight ducts there were pigment cylinders; extreme plethora of the surrounding area, and infiltration from annular cells and polynuclears. Forensic chemical analysis showed 12.8 mg of copper; 6.6 mg in the uterus and 5.6 mg in the kidneys. From data obtained it can be concluded that the patient died from cupric compound poisoning, complicated by interruption of the pregnancy and uterine hemolytic hemorrhage. It was later established that during the month before being admitted to the hospital the patient introduced a solution of blue vitriol into the uterine cavity to interrupt the pregnancy.
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PMID:[Fatal poisoning with blue vitriol]. 663 45

The antioxidant enzyme superoxide dismutase (SOD) found in the cytosol of eucaryotic cells and the plasma protein ceruloplasmin are copper containing proteins though to be important in providing protection from oxygen toxicity. To investigate the hypothesis that copper deficiency in the rat could result in decreased lung SOD activity and plasma ceruloplasmin concentration resulting in increased susceptibility to O2 lung damage, we performed a series of experiments exposing copper-deficient and control rats to normobaric and hyperbaric hyperoxia. Lung SOD activity in the copper-deficient rats was found to be 56% of control and ceruloplasmin content was 6% of control. The copper-deficient rats exhibited increased mortality and enhanced pulmonary toxicity as evidenced by increased pathologic damage and lung edema during the normobaric exposure to 85% O2. Copper-deficient animals also showed increased susceptibility to a hyperbaric exposure of 4 ata of 100% O2 with a decreased time of survival. The copper-deficient rat represents a new model for the study of oxidant injury.
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PMID:Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia. 672 91

After intraperitoneal injection of paraquat, rats showed evidence of neurologic and respiratory damage and had a mortality rate of 41% in 3 days. The lungs quadrupled in weight between the third and the fifth day. Pulmonary edema and extravascular fibrin and platelets were identified by light and transmission electron microscopy. As early as 4 h after injection of the paraquat, 51Cr from labeled platelets began accumulating in the lungs. The peak was reached by 48 h; 125I from labeled fibrinogen also concentrated in the lungs of treated rats. Total complement was unchanged. The paraquat-treated rat is a suitable model for study of the behavior of fibrin and platelets in permeability pulmonary edema. Disturbances of copper metabolism deserve further investigation.
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PMID:Accumulation of radionuclide-labeled platelets and fibrinogen in paraquat-damaged rat lungs. 708 18

Exposure of rats to hyperoxia or to treatment with endotoxin, increases lung manganese superoxide dismutase (MnSOD) gene expression. However, the paths by which these environmental signals are transduced into enhanced MnSOD gene expression are unknown. We now provide evidence that heterotrimeric G proteins are involved in the hyperoxia-induced increase in lung MnSOD gene expression but that pertussis toxin-sensitive G proteins are not involved in the endotoxin-induced elevation of lung MnSOD gene expression. We also show that treating rats with pertussis toxin decreased lung MnSOD activity approximately 50%. This decline in MnSOD activity occurred without a change in the lung activity of copper-zinc SOD, catalase, or glutathione peroxidase. In air-breathing rats, the pertussis toxin-induced decrease in MnSOD activity was associated with the development of lung edema, pleural effusion with a high concentration of protein, and biochemical evidence of lung oxygen toxicity. Compared to air-breathing rats, maintenance of pertussis toxin-treated rats under hypoxic or hyperoxic conditions respectively decreased or increased intrathoracic fluid. Endotoxin treatment elevated lung MnSOD activity and protected pertussis toxin-treated rats from an increase in intrathoracic fluid.
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PMID:Pertussis toxin treatment alters manganese superoxide dismutase activity in lung. Evidence for lung oxygen toxicity in air-breathing rats. 820 Sep 62

Acute pulmonary edema was assessed quantitatively in 12 experiments on six anesthetized dogs. Thirty-two copper foil electrodes were placed around each animal's thorax at the level of the third intercostal space. A real-time electrical impedance tomograph was used to form images of the electrical admittivity of the thorax in and near the plane of these electrodes. The lungs were identified by studying the change in admittivity associated with inspiration. Mean admittivity in these lung regions was assessed at 40-min intervals for the next 3-6 hours. In six control experiments, each having a duration of 200 min, the initial admittivity of the lung regions was 102 +/- 16(SD) mS/m. Lung admittivity usually increased during the first 80 min, and then remained within 2 mS/m of its value at 80 min for the remaining 120 min. In six experiments with pulmonary edema, an initial period of change followed by stability was observed. When stability had been attained, 0.07 ml/kg of oleic acid was injected slowly into a central venous site. Five animals received oleic acid, the sixth received a sham injection of saline. In the five receiving oleic acid, lung admittivity rose steadily for the remainder of the experiment. The increase in lung admittivity in these five animals was between 4 and 16 mS/m. In the sham injected experiment, the lung admittivity changed by 1 mS/m. We conclude that impedance imaging can provide semiquantitative assessment of the development of acute pulmonary edema.
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PMID:Assessment of acute pulmonary edema in dogs by electrical impedance imaging. 868 24


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