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

Although eugenol, the active phenolic constituent of oil of cloves, has been implicated as a cause of noncardiogenic pulmonary edema, the mechanism of lung injury is unknown. We studied the effects of intravenous infusion of eugenol in rats and found that 4 microliters and 8 microliters of eugenol (6.52 mol/L) caused acute respiratory distress with hemorrhagic pulmonary edema. Histologic features included perivascular, interstitial, and alveolar edema with extravasation of red blood cells and neutrophils into the alveolar space and alveolar capillary trapping of neutrophils. In addition, lungs treated with eugenol had increased bronchoalveolar lavage fluid (BALF) protein content, and lung wet-to-dry weight ratios were increased in animals treated with 8 microliters eugenol. Pretreatment with intravenous superoxide dismutase (SOD) or catalase but not dimethylthiourea (DMTU) decreased BALF protein content after infusion of 4 microliters and 8 microliters of eugenol. SOD and catalase but not DMTU decreased lung wet-to-dry weight ratios in animals infused with 8 microliters of eugenol. We conclude that intravenous infusion of eugenol causes hemorrhagic pulmonary edema with intrapulmonary sequestration of neutrophils and suggest that the injury may be at least partly oxidant mediated.
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PMID:Intravenous eugenol causes hemorrhagic lung edema in rats: proposed oxidant mechanisms. 784 74

Because fetal rat lungs have lower baseline levels of both surfactant and antioxidant enzymes than full-term newborn rats, we questioned whether prematurely delivered rats might be more susceptible to O2 toxicity than those born at term. In the present studies, prematurely delivered rats (gestational d 21 of 22) and full-term rat pups were simultaneously put in > 95% O2 after birth. Surprisingly, we found that the preterm rats were not more susceptible to O2-induced lung damage and lethality than full-term newborns, but, in fact, the composite percentage of survival was even greater in the preterm pups from 7 to 9 d in hyperoxia and were similar thereafter up to 14 d in high O2. In addition, the preterm rats showed significantly decreased lung wet/dry weight ratios and consistently less severe pathologic evidence of pulmonary edema compared with term rats at 6 and 8 d of O2 exposure. The premature pups demonstrated the capability of inducing pulmonary antioxidant enzyme responses to hyperoxia by 3 d, and had significantly elevated copper-zinc superoxide dismutase, catalase, and glutathione peroxidase activities (and lung surfactant contents) at 6 d of O2 exposure compared with the term rats in O2. The rates of lung total O2 consumption and cyanide-resistant O2 consumption at d 6 in hyperoxia were not different for preterm versus term pups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative responses of premature versus full-term newborn rats to prolonged hyperoxia. 816 59

Respiratory complications, especially pulmonary edema, account for over 50% of mortalities in inhalation injuries. This study was conducted to determine the effect of free radical scavengers and hyperbaric oxygen (HBO) in vivo on reducing pulmonary edema. Adult New Zealand rabbits were allowed to breath cooled, cotton smoke until a significant inhalation lung injury was produced. Five percent of body weight lactated Ringer's solution was then administered i.v. over 2 h. The following free radical scavengers were given as bolus infusions at the beginning of fluids resuscitation: superoxide dismutase, catalase, butylated hydroxytoluene/piperonyl butoxide, and mannitol. At the completion of fluid administration, half of the subjects were given HBO treatment. Pulmonary edema was then measured as extravascular lung water and wet/dry lung weight. Results indicate that free radical scavengers or HBO reduce pulmonary edema. Free radical scavengers in conjunction with HBO showed no significant improvement over HBO or free radical scavengers alone.
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PMID:Effect of radical scavengers and hyperbaric oxygen on smoke-induced pulmonary edema. 818 May 64

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

Pulmonary edema formation and the role of polymorphonuclear leukocytes (PMN) was evaluated during the generalized Shwartzman reaction (GSR) model in rabbits. Chemiluminescence (CL) and superoxide (O2-) production activity stimulated by FMLP were measured in circulating PMN after a single intravenous injection of endotoxin (E. coli 026:B6, 40 micrograms/kg) (E1). CL peaked at 36 hr after E1 injection and then decreased gradually to a normal range within 7 days. O2- production changed in a similar fashion. On the other hand, the PMN count peaked at 72 hr and remained at a high value until day 7. To induce GSR, a second venous injection of endotoxin (40 micrograms/kg) (E2) was administered 36 hr after the first one (E1). Four times as many PMN were observed in the lung capillaries 4 hr after the second endotoxin injection than after the first endotoxin injection (4 hr). The degree of lung edema formed increased after E2, but did not increase after E1. An alveolar hyaline-like exudate was observed 24 hr after E2. A continuous intravenous injection of superoxide dismutase (SOD) plus catalase or PMN depletion, prevented the development of post-E2 lung edema. If E2 was given 7 days after E1, no lung edema formed at all. These data indicate that oxygen free radicals from activated PMN by endotoxin play an important role in prolonged lung edema formation in the GSR model.
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PMID:Prolonged lung edema formation during the generalized Shwartzman reaction in rabbits--can it be a model for septic lung disease? 838 87

Diesel engine-powered vehicles emit some 30 to 100 times more particles than do gasoline engine cars. We previously reported that diesel exhaust particles (DEP) instilled intratracheally into mouse caused lung edema accompanying endothelial cell damage. In order to clarify further the biological effects of DEP on the respiratory system, the primary target of DEP instillation, we examined the direct action of DEP on isolated tissues and the cytotoxicity of DEP on cultured cells of respiratory tracts in guinea pigs. DEP were collected on glass fiber filters from a light-duty (2730 cc), four cylinder diesel engine. DEP induced a dose-dependent relaxation in tracheal smooth muscle and lung parenchymal preparations from guinea pigs. Neither propranolol nor ranitidine inhibited the relaxing effect of DEP on tracheal preparations. DEP also exhibited concentration- and time-dependent cytotoxicity on cultured tracheal smooth muscle cells and lung fibroblasts from guinea pigs, as assessed by specific [51Cr] release. These cytotoxicities induced by DEP were significantly inhibited by catalase, deferoxamine and MK-447, whereas SOD and mannitol had little effect. These inhibitory effects were blunted by the higher concentration of DEP. These results suggest that the cytotoxicity of DEP may cause dysfunction of respiratory tissues, which are mediated via oxygen radicals, probably hydroxyl radicals or hydrogen peroxides.
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PMID:Biological effects of diesel exhaust particles (DEP) on tissues and cells isolated from respiratory tracts of guinea pigs. 874 91

Reactive oxygen metabolites (ROMs) are thought to play a key role in the pathogenesis of the adult respiratory distress syndrome (ARDS). Accordingly, the use of ROM scavengers, such as N-acetyl-cysteine or dimethylthiourea, as therapeutic adjuncts to prevent oxidant-mediated damage to the lung have been evaluated extensively in animal models of ARDS. Results with this approach have been quite variable among studies. Another strategy that has been examined in animal models of ARDS is the administration of various enzymes, particularly superoxide dismutase (SOD) or catalase (CAT), in an effort to promote the conversion of ROMs to inactive metabolites. In theory, this strategy should be more effective than the use of ROM scavengers since a single molecule of a catalytically active molecule can neutralize a large number of molecules of a reactive species, whereas most scavengers act in a stoichiometric fashion to neutralize radicals on a mole-for-mole basis. This notion is supported by studies showing that prophylactic treatment with CAT provides impressive protection against acute lung injury induced in experimental animals by the administration of lipopolysaccharide (LPS). Results with SOD have been more variable. Recently, we have utilized a porcine model of LPS-induced ARDS to investigate the therapeutic potential of EUK-8, a novel, synthetic, low molecular salen-manganese complex that exhibits both SOD-like and CAT-like activities in vitro. Using both pre- and post-treatment designs, we have documented that treatment with EUK-8 significantly attenuates many of the features of LPS-induced acute lung injury, including arterial hypoxemia, pulmonary hypertension, decreased dynamic pulmonary compliance, and pulmonary edema. These findings support the view that salen-manganese complexes warrant further evaluation as therapeutic agents for treatment or prevention of sepsis-related ARDS in humans.
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PMID:Role of oxidant stress in the adult respiratory distress syndrome: evaluation of a novel antioxidant strategy in a porcine model of endotoxin-induced acute lung injury. 882 94

Isolated rat lungs subjected to hypoxia-reoxygenation (H/R) were used to study NO-mediated pulmonary vasodilation during oxidant-induced vascular injury. After ventilation with 3% O2, reoxygenation with 21% (H/R 21%) or 95% O2 (H/R 95%) caused lung edema and lipid peroxidation. Vasodilation to A23187 was attenuated after H/R 21% and abolished after H/R 95%. The vasodilator-response curve to NO was more shifted to the right after H/R 95% than after H/R 21%. Pretreatment with superoxide dismutase (SOD; 150 U/ml) and catalase (120 U/ml) prevented impairment of A23187- and NO-mediated vasodilation. SOD and catalase added after reoxygenation restored vasodilation to NO but not to A23187. In lungs obtained from chronically hypoxic rats but studied under conditions of normoxic ventilation, vasodilation to A23187 was abolished, but vasodilation to NO remained unchanged. The data suggest that generation of oxygen-derived reactive species after H/R produces impairment of NO formation as well as direct inactivation of NO. This does not explain the decreased endothelial NO-mediated pulmonary vasodilation in chronically hypoxic rats.
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PMID:Hypoxia-reoxygenation impairs NO-mediated vasodilation in rat lungs. 884 93

Fumonisin B1 (FB1) causes equine leukoencephalomalacia, porcine pulmonary edema, and liver tumors and chronic nephritis in rats. To investigate mechanisms by which FB1 induces toxicity, effects of FB1 on cellular glutathione (GSH) redox status and GSH depletion on FB1 toxicity in pig kidney (LLC-PK1) cells were studied. Treatment of LLC-PK1 cells with 50 microM FB1 for 24 hours significantly decreased cellular GSH contents from 56 +/- 3.2 to 42.7 +/- 4.4 nmol/mg protein (p < 0.05) and increased the activities of glutathione reductase (GR) from 25.7 +/- 2.4 to 35.7 +/- 5.0 mumol NADPH/mg protein (p < 0.05). The activities of glutathione peroxidase (GSHpx), catalase, and Cu,Zn-superoxide dismutase (SOD) were not changed by this treatment. Treatment of LLC-PK1 cells for 12 hours with 0.1 mM buthionine sulfoximine (BSO), a selective inhibitor of the enzyme gamma-glutamylcysteine synthetase that catalyzes the rate-limiting reaction in de novo GSH synthesis, decreased cellular GSH levels to about 20% of that found in the control cells. The cells pretreated with 0.1 mM BSO for 12 hours were significantly sensitized to the FB1 cytotoxicity as determined by a long-term survival assay (p < 0.05). The results demonstrate that FB1 changes GSH redox cycle status in LLC-PK1 cells, and GSH may play a role in cytoprotection against FB1 toxicity.
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PMID:Alterations of the glutathione redox cycle status in fumonisin B1-treated pig kidney cells. 902 70

Pulmonary edema develops when pulmonary blood flow is interrupted, then restored. Because the lung is not always hypoxic when ischemic, mechanisms of pulmonary ischemia-reperfusion injury are likely to differ from systemic organs, where reactive oxygen species generated during reperfusion mediate organ dysfunction. We previously showed that pulmonary vascular permeability of isolated ferret lungs increased prior to reperfusion, if ventilation was maintained while blood flow was impaired. To determine whether reactive oxygen metabolites generated during ischemia mediated ischemic injury, we measured tissue levels of F2-isoprostanes as an index of lipid peroxidation, 30 min after administration of glucose (5 mM)-glucose oxidase (GOX, 0.1 U/ml), or after short (45 min) or long (180 min) ventilated ischemia, in isolated ferret lungs. Osmotic reflection coefficient for albumin (sigma alb), an estimate of vascular protein permeability, was measured in the same lungs. Tissue F2-isoprostanes increased 375% after exposure to glucose-GOX in association with a 42% decrease in sigma alb, and administration of catalase (CAT, 100,000 U) and superoxide dismutase (SOD, 25,000 U) completely attenuated this lipid peroxidation. In contrast, tissue F2-isoprostanes increased only 60% following 45 min of ischemia, then did not increase additionally. sigma alb was not altered by 45 min of ischemia, but decreased 72% following 180 min of ischemia. CAT+SOD did not alter F2-isoprostane formation during ischemia, but partially attenuated vascular injury. These results suggest that tissue levels of F2-isoprostanes reflect lung lipid peroxidation, but that F2-isoprostane generation does not directly increase vascular permeability following ventilated pulmonary ischemia.
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PMID:F2-isoprostane generation in isolated ferret lungs after oxidant injury or ventilated ischemia. 980 Oct 71


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