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

B6.A.D. (Ahr(d)/Nat(s)) mice were utilized to investigate the short-term pulmonary response to JP-8 jet fuel (JP-8) aerosol inhalation. Mice were nose-only exposed to atmospheres of 0 to 118 mg/m3 for 1 h/d over a period of 7 days to further test the hypothesis that JP-8 concentrations below the permissible exposure level (PEL) of 350 mg/m3 will induce lung injury. At 24 to 30 hours after the final exposure, pulmonary function and respiratory permeability were measured on anesthetized mice and then randomly assigned for bronchoalveolar lavage or histopathology. Bronchoalveolar lavage fluid (BALF) was analyzed for total protein, lactic dehydrogenase (LDH), N-acetyl-beta-D-glucosaminidase (NAG), and cytology. Respiratory permeability increases were observed following doses of 48 and 118 mg/m3 and were supported by concomitant BALF increases in total protein and LDH. Conversely, NAG and alveolar macrophage levels decreased following the same exposure concentrations. Morphological lung injury was characterized by the targeting of bronchiolar epithelium and consisted of perivascular edema, Clara cell vacuolization, and necrosis. Alveolar injury included sporadic pulmonary edema, intra-alveolar hemorrhage, and alterations in type II epithelial cells. These results indicate that repeated inhalation of aerosolized JP-8 induces physiological, biochemical, cellular, and morphological lung injury. This study also provides evidence for the reevaluation of the 350 mg/m3 PEL for more volatile petroleum distillates with regard to respirable aerosols.
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PMID:Short-term pulmonary response to inhaled JP-8 jet fuel aerosol in mice. 1102

Fumonisin B1 is a mycotoxin commonly found on corn. It is hepatotoxic and nephrotoxic in domestic and experimental animals, and causes equine leukoencephalomalacia and porcine pulmonary oedema. It is a potent inhibitor of ceramide synthase. Inhibition leads to accumulation of free sphingoid bases in cells and tissues. In pig kidney epithelial cells (LLC-PK1), fumonisin B1 induces increased tumour necrosis factor alpha (TNFalpha) expression independent of the accumulation of sphingoid bases. The objective of this study was to investigate pharmacological approaches for intervening in fumonisin B1 toxicity using the LLC-PK1 cell model. The toxicity of fumonisin B1 was assayed using cell viability and lactate dehydrogenase (lactate dehydrogenase) release. Pretreatment of cells with myriocin, preventing sphinganine accumulates, prevented the fumonisin B1-induced decrease in cell viability and increased lactate dehydrogenase release. Modulation of adenosine receptor activity did not reduce the fumonisin B1 cytotoxicity. As with myriocin, silymarin pretreatment prevented the fumonisin B1-induced effects on cell viability and lactate dehydrogenase release. When added 6 or 24 hr after treatment of cells with fumonisin B1, both myriocin and silymarin reversed the decreased cell viability and suppressed the increased lactate dehydrogenase release. Myriocin, but not silymarin, blocked the accumulation of sphinganine in fumonisin B1-treated cells. Silymarin, unlike myriocin, induced expression of TNFalpha to an extent similar to fumonisin B1, but pretreatment with silymarin decreased the fumonisin B1-induced TNFalpha expression in LLC-PK1 cells. Results suggest that the mechanisms by which myriocin and silymarin protect renal cells are different, and silymarin potentially prevents fumonisin B1-induced toxicity by modulating TNFalpha expression or signals downstream of the inhibition of ceramide synthase.
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PMID:Pharmacological antagonism of fumonisin B1 cytotoxicity in porcine renal epithelial cells (LLC-PK1): a model for reducing fumonisin-induced nephrotoxicity in vivo. 1207 8

We investigated the pharmacologic effects of the antioxidant Vitamin E (alpha-tocopherol [alpha-toc]) in airway inflammation induced by inhaled endotoxin. A preparation of alpha-toc incorporated in liposomes was administered intraperitoneally in mice 1 h after exposure of aerosolized endotoxin. Injection of 50 mg alpha-toc/kg significantly decreased the number of neutrophils in airspaces and prevented lung injury, monitored both as decreased lactate dehydrogenase activity in airways and reduced lung edema when compared with animals treated with plain liposomes. Immunofluorescence staining of lung tissue revealed that treatment with alpha-toc decreased the number of neutrophils in lung interstitium, whereas the number in lung blood vessels and peripheral blood did not differ between mice treated with alpha-toc and control mice. Our results indicate that alpha-toc downmodulates the migration of neutrophils across the endothelial barrier, but in contrast to strong anti-inflammatory drugs such as corticosteroids, without inhibition of transcription factors involved in the early inflammatory response (nuclear factor-kappaB/activator protein-1). Neither was the endotoxin-induced expression of proinflammatory cytokines in lung tissue downregulated. Treatment with a combination of alpha-toc and a suboptimal dose of 0.5 mg/kg dexamethasone enhanced the effect, suggesting that alpha-toc, in combination with low doses of corticosteroids, might be effective for therapeutic treatment of acute lung injury.
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PMID:Vitamin E reduces transendothelial migration of neutrophils and prevents lung injury in endotoxin-induced airway inflammation. 1254 Apr 87

Influenza is a respiratory tract disease of viral origin that can cause major epidemics in humans. The influenza virus infects and damages epithelial cells of the respiratory tract and causes pneumonia. Lung lesions of mice infected with influenza virus resembles those seen in humans with influenza, and can result in severe and even fatal pneumonia. In contrast, experimental infection of rats with the virus induces a milder form of the disease, with no mortality. The purpose of the study reported here was to determine the time course of influenza infection and lung injury in Brown Norway (BN), Fischer-344 (F344), and Sprague-Dawley (SD) rats to ascertain whether genetic background impacts susceptibility to infection and host responses. Rats of each strain were inoculated intranasally with 10,000 plaque-forming units of rat-adapted influenza virus (RAIV), and lungs were assessed at postinoculation hour (PIH) 2, 24, 48, 72, and 144 for viral titer, inflammatory cells, pro-inflammatory cytokines, and biochemical indicators of lung edema (protein) and injury (lactate dehydrogenase [LD] activity). Virus titer peaked at PIH 24, and was 100-fold higher in the F344 and SD, compared with the BN strain. Alveolar macrophages, LD activity, and total protein concentration were higher in the BN rats, whereas neutrophil numbers and interleukin 6 and tumor necrosis factor-alpha activities were greatest in the bronchoalveolar lavage fluid of F344 and SD rats. The results indicate that F344 and SD rats respond in similar manner to viral infection, whereas viral replication was more limited in BN rats and was associated with a different profile of pulmonary cells.
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PMID:Kinetic profile of influenza virus infection in three rat strains. 1286 75

Alveolar hemorrhage and pulmonary edema induced by mechanical ventilation are partly dependent on cardiac output. Because cardiac output is low during hypothermia, we hypothesized that hypothermia may protect against these vascular manifestations of ventilator-induced lung injury. Twenty-seven Sprague-Dawley rats were assigned to either normothermia (37 +/- 1 degrees C)-injurious ventilation (NT; n = 10), hypothermia (27 +/- 1 degrees C)- injurious ventilation (HT; n = 10), or nonventilated control ( n = 7). The two ventilated groups were subjected to injurious ventilation of peak airway pressure 30 cm H(2)O with zero end-expiratory pressure for 20 min. Compared with the NT group, the hemorrhage/congestion score of the lung (11.2 +/- 1.5 vs. 4.7 +/- 1.6; p < 0.001) and the ratio of wet/dry lung weight (6.1 +/- 0.8 vs. 5.0 +/- 0.1; p = 0.046) of the HT group were lower. Compared with the NT group, protein concentration (3,471 +/- 1,985 micro g/ml vs. 1,374 +/- 726 micro g/ml; p = 0.003) and lactate dehydrogenase level (0.43 +/- 0.22 U/ml vs. 0.18 +/- 0.1 U/ml; p = 0.046) in bronchoalveolar lavage fluid of the HT group were lower. Whereas pressure-volume curve was shifted to the right in the NT group after injurious ventilation, it was not shifted in the HT group. In conclusion, hypothermia in rats attenuated the degrees of vascular manifestations and alveolar epithelial injuries induced by injurious ventilation, and preserved the mechanical properties of the lung.
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PMID:Hypothermia attenuates vascular manifestations of ventilator-induced lung injury in rats. 1287 37

Lung inflammation is a key response to increased levels of particulate air pollution (PM); however, the cellular mechanisms leading to this response are poorly understood. To determine whether oxidants are implicated in PM-dependent lung inflammation, we tested the ability of N-acetylcysteine (NAC) to prevent lung inflammation in a rat model of short-term exposure to concentrated ambient particles (CAPs). Adult Sprague-Dawley rats were exposed to either CAPs aerosols (CAPs mass concentration 1060 +/- 300 microg/m(3)) or filtered air (Sham controls) for 5 h. NAC-treated rats received 50 mg/kg (ip) NAC 1 h prior to exposure to CAPs. Oxidative stress and recruitment of inflammatory cells into bronchoalveolar lavage were evaluated 24 h after removal of the animals from the exposure chamber. Rats breathing CAPs aerosols showed significant oxidative stress, determined by the accumulation of thiobarbituric reactive substances (TBARS, 90 +/- 15 pmol/mg protein; sham control: 50 +/- 5 pmol/mg protein, p < 0.02) and oxidized proteins (1.6 +/- 0.4 nmol/mg protein, sham: 0.70 +/- 0.02 nmol/mg protein, p < 0.01) in their lungs. CAPs-induced oxidative stress was associated with increased numbers of polymorphonuclear leukocytes in bronchoalveolar lavage (BAL) (9 +/- 2%; sham: 1.6 +/- 0.5%, p < 0.001) and slight lung edema (wet/dry ratio: 4.77 +/- 0.03, sham: 4.69 +/- 0.02). No significant change was found in BAL protein concentration, total cell count, or lactate dehydrogenase (LDH) activity. NAC pretreatment effectively prevented CAPs-induced TBARS accumulation (30 +/- 10 pmol/mg protein, p < 0.006), lung edema (4.64 +/- 0.08, p < 0.05), and polymorphonuclear neutrophil (PMN) influx into the lungs (2.1 +/- 0.5%, p < 0.001), but did not alter the protein carbonyl content. Histological evaluation of tissue samples confirmed the BAL findings. CAPs-exposed animals showed slight bronchiolar inflammation and thickened vessels at the bronchiole, whereas NAC treated animals showed no histological alterations. Regression analyses showed strong associations between increased TBARS accumulation and the CAPs content of Al, Si, and Fe, and trends of association between carbonyl content and Cr and Na concentrations, and between BAL PMN count and Cr, Zn, and Na. These data demonstrate that oxidants are critical mediators of the inflammatory response elicited by PM inhalation.
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PMID:N-acetylcysteine prevents lung inflammation after short-term inhalation exposure to concentrated ambient particles. 1505 6

Pulmonary fibrosis is a common consequence of numerous pulmonary diseases. The current therapeutic approaches for this condition are unsatisfactory. Feitai, a composite formula consisting of several herbs, is used in China as a folk remedy for treating patients with pulmonary tuberculosis. In this study, we extensively investigate the effects and mechanisms of Feitai on bleomycin (BLM)-induced pulmonary fibrosis in rats. One hundred and twenty male Sprague-Dawley rats were randomly divided into four groups, referred to as the saline-water, saline-Feitai, BLM-water, and BLM-Feitai groups. Following a single instillation of BLM (5 mg/kg) or saline, rats were orally administered Feitai at a dose of 3 g/kg body weight or sterilized distilled water once daily. Rats were killed at 7, 14, or 28 d post-BLM. Inflammatory cell count, protein concentration, and lactate dehydrogenase activity in bronchoalveolar lavage fluid were measured, and myeloperoxidase activity and lipid peroxide content in lung homogenates were analyzed. Treatment with Feitai inhibited lung fibrotic progression induced by BLM, as indicated by the decrease in lung hydroproline content and lung fibrosis score at 28 d post-BLM. This was accompanied by significant amelioration of BLM-induced body weight loss, lung edema, and inflammatory response during the development of lung injury in the acute phase. The results strongly indicate the beneficial effects of Feitai in protecting against BLM-induced pulmonary fibrosis. Furthermore, the inflammatory response and lipid peroxidation were inhibited by Feitai, suggesting that the effect of this formula on BLM-induced lung injury and fibrosis is associated with antiinflammatory and antioxidant properties.
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PMID:Feitai attenuates bleomycin-induced pulmonary fibrosis in rats. 1513 36

Massive hepatic infarction associated with pregnancy is extremely rare, but is potentially fatal. A 35-year-old primigravida with mild preeclampsia developed acute right upper quadrant pain and marked elevation of liver enzymes at 26 weeks' gestation. After emergent cesarean section, her condition was complicated by oliguric renal failure and pulmonary edema with further deterioration of hepatic function (aspartate transaminase 4339 IU/L; alanine transaminase 3489 IU/L; lactate dehydrogenase 10780 IU/L). The contrast-enhanced computed tomography revealed non-enhancing low attenuation throughout the right lobe of liver, compatible with infarction. Continuous hemodiafiltration was initiated as renal support on postpartum day one. However, excessive fluid accumulation persisted, and she developed severe edema formation in both lung and systemic body surface. To ameliorate microvascular endothelial injury, corticosteroid therapy was begun on postpartum day five. Following treatment initiation, her renal and hepatic function showed steady improvement, accompanied by drastic resolution of edema formation. She was discharged five weeks postpartum with no additional treatment, and is without sequelae six months later. Massive hepatic infarction should be considered in preeclamptic patients who present acute abdominal pain and severe hepatic dysfunction, and continuous hemodiafiltration with corticosteroid therapy may improve the maternal outcome.
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PMID:Massive hepatic infarction in preeclampsia: successful treatment with continuous hemodiafiltration and corticosteroid therapy. 1549 25

Ceramide is a lipid second messenger that was recently identified as mediator of pulmonary edema in vivo. Here, we investigated the effect of ceramide on the permeability of confluent endothelial cell monolayers. In monolayers of bovine pulmonary artery and human microvascular pulmonary endothelial cells, incubation with C6-ceramide for 3 h elevated permeability in a concentration-dependent manner, whereas dihydroceramide was without effect. After 3 h of incubation with ceramide, we found no signs of necrosis (release of lactate dehydrogenase, loss of thiazylyl blue reduction) or apoptosis (ssDNA, caspase-8 activity). The increased endothelial permeability in response to ceramide was attenuated by the Ser/Thr protein kinase inhibitors K252a, K252b and H-7, as well as by the phosphatidylinositol-specific phospholipase C inhibitor L108. Since in some systems sphingosine-1-phosphate (S1P) acts antagonistic to ceramide, the effect of S1P was studied. S1P transiently increased endothelial cell resistance, whether it was given together with ceramide or 90 min thereafter. These data provide a novel example of the antagonism between S1P and ceramide. Our findings further suggest that ceramide alters vascular permeability by activation of pathways dependent on unidentified phospholipase C and Ser/Thr kinase isoenzymes.
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PMID:Ceramide alters endothelial cell permeability by a nonapoptotic mechanism. 1573 57

We analyzed the clinical characteristics, complications, severity, and maternal and fetal survival of patients suffering from HELLP syndrome (Hemolysis, Elevated Liver enzymes level, Low Platelet count) requiring admission to the intensive care unit in four hospitals from Buenos Aires area, Argentina. Data was revised in the charts from March 1997 to March 2003 and 62 patients were included in the study. During the second half of pregnancy or immediate puerperal period, diagnostic criteria were defined on the basis of preeclampsia and the following laboratory abnormalities: platelet count nadir <150,000/mm3, serum hepatic aminotransferases >70 UI/l, and serum lactic dehydrogenase >600 UI/l, total bilirubin >1.2 mg/dl and/or periferical blood smear with hemolysis. The mean maternal age was 28 +/- 8 years; parity 2.7 +/- 2.3; gestational age 33 +/- 4 weeks. According to platelet count, 23 cases were identified to class 1, 29 to class 2 and the rest to Martin's class 3. There were 16 eclamptic patients. The platelet count was 67,604 +/- 31,535/mm3; alanine aminotransferase 271 +/- 297 UI/l; aspartate aminotransferase 209 +/- 178 UI/l; serum lactic dehydrogenase 1444 +/- 1295 UI/l; serum creatininine levels 1.1 +/- 0.8 mg/dl. Forty-one patients had diverse degree of renal function damage, renal dialysis and plasmapheresis was required in one female. Respiratory failure due to pulmonary edema was observed in four patients. All obstetric patients survived. There were four perinatal deaths. In our population sample, low rate of life-threatening maternal complications and low perinatal mortality were observed.
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PMID:[Maternal morbidity and perinatal mortality in HELLP syndrome. Multicentric studies in intensive care units in Buenos Aires area]. 1583 Jul 88


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