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)

We report a case of acute inhalation injury of nitric acid in a 56-year old white male. The patient presented conscious and dyspnoic at the emergency department after cleaning a copper chandelier with nitric acid. He had to be intubated 2 h after admission and mechanically ventilated because of fulminant respiratory insufficiency. As all sources of mechanical ventilation failed, extracorporeal membrane oxygenation had to be established 7 h after admission. With the additional use of surfactant and low dose inhalation therapy with nitric oxide (NO), the patient could be stabilised for 3 days and lung function improved temporarily. Despite all efforts the patient died at the fourth day from refactory respiratory failure. Pathologic examination revealed massive pulmonary edema without signs of inflammation. Thus, nitric acid inhalation induced pulmonary edema appears to be a most severe situation in which even most modern therapeutic interventions fail. As, in respect of recent literature and our case no promising therapy for nitric acid inhalation pulmonary edema is available, our efforts have to be directed towards prevention of nitric acid exposure.
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PMID:Fatal pulmonary edema after nitric acid inhalation. 925 58

The mechanism by which pertussis toxin (Ptx) causes lung edema is not clear. We investigated the role of pulmonary manganese superoxide dismutase (MnSOD) and protein kinase C (PKC) in Ptx-induced lung edema. We demonstrated that intraperitoneal injection of Ptx at a concentration of 5 microg/100 g body weight caused a similar degree of lung edema in 2 d, as measured by lung wet weight/dry weight ratio, in heterozygous MnSOD gene (Sod2)-knockout mice (Sod2(+/-)) and in their wild-type littermates (Sod2(+/+)). The level of lung MnSOD activity in Sod2(+/-) mice was approximately half that of Sod2(+/-) mice. Ptx had no effect on levels of lung MnSOD messenger RNA, immunoreactive protein, or enzyme activity in either Sod2(+/+) or Sod2(+/-) mice. Ptx also had no effect on lung copper-zinc SOD, catalase, and glutathione peroxidase activities in these mice. On the other hand, Ptx caused the activation of lung PKC, for example, by translocation of a 72-kD PKC isoform from the cytosolic fraction to the membrane fraction. Pretreatment of mice with bisindolylmaleimide, a PKC inhibitor, prevented both the Ptx-induced activation of PKC and lung edema. These data suggest that Ptx-induced lung edema in mice is, at least in part, due to the activation of lung PKC.
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PMID:Pertussis toxin-induced lung edema. Role of manganese superoxide dismutase and protein kinase C. 1003 Aug 45

The antioxidant and anti-inflammatory activities of two transition metal complexes of bioflavonoid rutin, Fe(rut)Cl(3) and Cu(rut)Cl(2), were studied. It was found that Cu(rut)Cl(2) was a highly efficient in vitro and ex vivo free radical scavenger that sharply decreased (by 2-30 times compared to the parent rutin): oxygen radical production by xanthine oxidase, rat liver microsomes, and rat peritoneal macrophages; the formation of thiobarbituric acid-reactive products in microsomal lipid peroxidation; and the generation of oxygen radicals by broncho-alveolar cells from bleomycin-treated rats. The copper-rutin complex was also a superior inhibitor of inflammatory and fibrotic processes (characterized by such parameters as macrophage/neutrophil ratio, wet lung weight, total protein content, and hydroxyproline concentration) in the bleomycin-treated rats. The antioxidant activity of Fe(rut)Cl(3) was much lower and in some cases approached that of rutin. Fe(rut)Cl(3) also stimulated to some degree spontaneous oxygen radical production by macrophages. We suggested that the superior antioxidant and anti-inflammatory activity of the copper-rutin complex is a consequence of its acquiring the additional superoxide-dismuting copper center. The inhibitory activity of Fe(rut)Cl(3) was lower, probably due to the partial reduction into Fe(rut)Cl(2) in the presence of biological reductants; however, similarly to the copper-rutin complex, this complex efficiently suppressed lung edema.
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PMID:Enhancement of antioxidant and anti-inflammatory activities of bioflavonoid rutin by complexation with transition metals. 1126 52

The experience of the Utrecht State University with postcoital estrogens in high and low combined doses and with postcoital placement of IUDs since 1964 with over 4000 patients is summarized. The high dose postcoital estrogen treatment consists of 5 mg ethinyl estradiol for 5 days, either orally, or in case of vomiting not controlled by an antiemetic, estradiol benzoate 30 mg by injection. Side effects recorded in 3016 women were nausea in 54%, vomiting in 24%, tender breasts in 23%, menorrhagia in 11%, altered cycle length in 24%. Complications were 1 case of non-fatal pulmonary edema and 1 case of an 8 kg weight gain during treatment. There were 3 pregnancies. The overall failure rate in the whole series was 0.15%, with 10% ectopic pregnancies. There were no thromboembolisms or teratogenic effects. The combined estrogen treatment consisted of 50 mc ethinyl estradiol with 250 mc levonorgestrel (Neogynon oral contraceptive), 2 pills followed by 2 pills 12 hours later. A double-blind randomized trial resulted in no significant differences in pregnancy rates or side effects between the high and low dose regimens. The alternate treatment, if the woman presents more than 72 hours after intercourse, or if estrogens are contraindicated, is postcoital insertion of an IUD. The Dept. of Obstetrics and Gynecology does not place an IUD in a woman with infection nor in case of rape unless there is time for a complete work-up. Nulliparas are informed of the increased risk of pelvic inflammatory disease. Recently, the Multiload-copper 250 and later ML 375 were used exclusively, to achieve better blastocidal effect and lower expulsion rates. The ethical debate over use of postcoital methods centers around the morality of "procuring a miscarriage," but this argument is not relevant since these methods will not terminate a pregnancy once implantation has occurred. In the Netherlands, 25% of all abortion clients become pregnant during their 1st intercourse. In 1982, 35,000 postcoital contraceptives were administered, (roughly 16% of all pregnancies), compared to 15,000 abortions (7% of pregnancies; a total of 23% of pregnancies terminated). Compare these figures with 29% unwanted pregnancies all terminated by abortion in Sweden in that year. The postcoital methods are cheap, effective, and invaluable in emergency cases of rape, incest, intoxication, failure of barrier contraceptives, or unwanted pregnancy in women fearful or opposed to abortion.
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PMID:Post coital contraception. 1226 14

An important issue in critical care medicine is the identification of ways to protect the lungs from oxygen toxicity and reduce systemic oxidative stress in conditions requiring mechanical ventilation and high levels of oxygen. One way to prevent oxygen toxicity is to augment antioxidant enzyme activity in the respiratory system. The current study investigated the ability of aerosolized extracellular superoxide dismutase (EC-SOD) to protect the lungs from hyperoxic injury. Recombinant human EC-SOD (rhEC-SOD) was produced from a synthetic cassette constructed in the methylotrophic yeast Pichia pastoris. Female CD-1 mice were exposed in hyperoxia (FiO2>95%) to induce lung injury. The therapeutic effects of EC-SOD and copper-zinc SOD (CuZn-SOD) via an aerosol delivery system for lung injury and systemic oxidative stress at 24, 48, 72 and 96 h of hyperoxia were measured by bronchoalveolar lavage, wet/dry ratio, lung histology, and 8-oxo-2'-deoxyguanosine (8-oxo-dG) in lung and liver tissues. After exposure to hyperoxia, the wet/dry weight ratio remained stable before day 2 but increased significantly after day 3. The levels of oxidative biomarker 8-oxo-dG in the lung and liver were significantly decreased on day 2 (P<0.01) but the marker in the liver increased abruptly after day 3 of hyperoxia when the mortality increased. Treatment with aerosolized rhEC-SOD increased the survival rate at day 3 under hyperoxia to 95.8%, which was significantly higher than that of the control group (57.1%), albumin treated group (33.3%), and CuZn-SOD treated group (75%). The protective effects of EC-SOD against hyperoxia were further confirmed by reduced lung edema and systemic oxidative stress. Aerosolized EC-SOD protected mice against oxygen toxicity and reduced mortality in a hyperoxic model. The results encourage the use of an aerosol therapy with EC-SOD in intensive care units to reduce oxidative injury in patients with severe hypoxemic respiratory failure, including acute respiratory distress syndrome (ARDS).
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PMID:Aerosolized human extracellular superoxide dismutase prevents hyperoxia-induced lung injury. 2204 89


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