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)

To the best of our knowledge, no case of ether-induced acute respiratory distress syndrome (ARDS) has been published as yet. A 36-year-old female developed pneumonitis which showed all the characteristics of a chemical-associated ARDS due to intravenous self-administration of ether: the hemodynamic investigation demonstrated a normal blood flow pattern with low left-heart filling pressure while the anteroposterior roentgenogram evidenced disseminated bilateral lung edema. Advanced symptomatic respiratory support including inhaled nitric oxide and steroidal anti-inflammatory use was the treatment of choice.
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PMID:Near fatal respiratory distress following massive ether intravenous injection. 1022 81

It was recently proposed that nitric oxide (NO) inhalation interferes with polymorphonuclear neutrophil (PMN) activation status during acute pulmonary inflammation, although variable results have been observed considering timing of NO administration, species, and model differences. After intratracheal administration of lipopolysaccharide (LPS) in rats, we characterized pulmonary inflammatory reaction (lung wet, dry, and wet to dry weights) and, using flow cytometry, the activation status (H2O2 production and beta2 integrin CD11b/CD18 expression) of PMN obtained from blood and from bronchoalveolar lavage (BAL). Eight hours after LPS injection, rats received for an additional 10 h, at a same Fio2 (85%), either 15 parts per million NO or the same gas flow of nitrogen. We found that 18 h after LPS, lung wet, dry, and wet-to-dry weights, H2O2 production, and CD11b/CD18 expression were increased. PMN obtained from BAL were highly activated as evidenced by an already maximal expression of the beta2 integrin CD11b/CD18, whereas the high H2O2 production at basal state could be further enhanced after ex vivo stimulation. Blood PMN were not different from control cells at basal state; however, their increased capacity to be stimulated ex vivo suggested an in vivo priming effect of intratracheal LPS. In conclusion, inhaled NO, given with a high FiO2, in the presence of this established endotoxinic lung injury did not reverse the markers of PMN activation studied nor lung edema formation in this rat model.
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PMID:Alveolar neutrophil oxidative burst and beta2 integrin expression in experimental acute pulmonary inflammation are not modified by inhaled nitric oxide. 972 80

The present study was designed to investigate the role of cytokines in the pathogenesis of Babesia caballi in experimentally infected horses. The expression of cytokine mRNA was determined by using reverse transcription-polymerase chain reaction in two B. caballi-infected horses for 2 weeks after the infection. In one horse, there was up-regulation of interferon-gamma, tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 mRNAs, while in the second horse, expression of only TNF-alpha mRNA was up-regulated. No change was observed in interleukin-4 mRNA in both of the horses. To know the relation between nitric oxide (NO) production and pathogenesis, NO production was assayed in three dexamethasone treated-B. caballi-infected horses. Production of NO in all 3 horses increased significantly before death, although the parasitemia level remained very low. Treatment with NO inhibitor resulted in the suppression of NO production and increased parasitemia level in a horse, which died of the infection. The pathological examination showed that the main cause of the death was dyspnoea and pulmonary edema. Histopathologically, diffuse global mesangial proliferative glomerulonephritis was also observed. These results suggested that NO may be a critical effector molecule of immune defense against parasite. TNF-alpha and NO might be contributing to the pathogenesis in B. caballi infection.
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PMID:Pathogenesis of Babesia caballi infection in experimental horses. 981 67

CAP18 (cationic antimicrobial protein; 18 kDa) is a neutrophil-derived protein that can bind to and inhibit various activities of lipopolysaccharide (LPS). The 37 C-terminal amino acids of CAP18 make up the LPS-binding domain. A truncated 32-amino-acid C-terminal fragment of CAP18 had potent activity against Pseudomonas aeruginosa in vitro. We studied the antimicrobial and LPS-neutralizing effects of this synthetic truncated CAP18 peptide (CAP18106-137) on lung injury in mice infected with cytotoxic P. aeruginosa. To determine its maximal effect, the CAP18106-137 peptide was mixed with bacteria just prior to tracheal instillation, and lung injury was evaluated by determining the amount of leakage of an alveolar protein tracer (125I-albumin) into the circulation and by the quantification of lung edema. The lung injury caused by the instillation of 5 x 10(5) CFU of P. aeruginosa was significantly reduced by the concomitant instillation of CAP18106-137. However, the administration of CAP18106-137 alone, without bacteria, induced lung edema, suggesting that it has some toxicity. Also, the peptide did not significantly reduce the number of bacteria that had been simultaneously instilled, nor did it significantly improve the survival of the infected mice. The addition of CAP18106-137 to aztreonam along with the bacteria did decrease the level of antibiotic-induced release of inflammatory mediators including tumor necrosis factor alpha, interleukin-6, and nitric oxide and also improved the survival of the mice. Therefore, more investigations are needed to confirm the toxicities and the therapeutic benefits of CAP18106-137 as an adjunctive therapy to antibiotics in the treatment of infections caused by gram-negative bacteria.
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PMID:Evaluation of antimicrobial and lipopolysaccharide-neutralizing effects of a synthetic CAP18 fragment against Pseudomonas aeruginosa in a mouse model. 983 25

We investigated the influence of HMR 3004, a new ketolide antibiotic, on the pulmonary inflammation induced by heat-killed fluorescein isothiocyanate-labeled Streptococcus pneumoniae. HMR 3004 downregulated (P < 0.05) the pneumococcus-induced release of interleukin-6 (IL-6), IL-1beta, and nitric oxide in bronchoalveolar lavage fluid. The drug limited (P < 0.05) neutrophil recruitment to lung tissues and alveoli but did not interfere with phagocytosis. HMR 3004 totally abrogated lung edema. By reducing inflammation in addition to possessing antimicrobial properties, HMR 3004 may participate in improving the outcome of bacterial pneumonia.
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PMID:Immunomodulating effects of HMR 3004 on pulmonary inflammation caused by heat-killed Streptococcus pneumoniae in mice. 983 35

We have used mice rendered deficient for nitric oxide synthase 2 (NOS2) production to study the role of inducible nitric oxide (NO) in the pathogenesis of allergic airways disease. Using a model with OVA as aeroallergen, we show that the manifestations of disease, including infiltration of inflammatory cells, particularly eosinophils, loss of structural integrity of the airway walls, microvascular leakage, pulmonary edema, and airway occlusion are markedly less severe in the NOS2 mutants than in wild-type animals. Indeed, NOS2-deficiency resulted in a 55-60% reduction in both circulatory and pulmonary eosinophil numbers following aeroallergen treatment, although eosinophil maturation or efflux from the bone marrow was not suppressed. There were no obvious differences in levels of airway hyperreactivity recorded in OVA-treated wild-type and NOS2-deficient mice. Interestingly, the suppression of allergic inflammation was accompanied by marked increases in T cell production of IFN-gamma but not by any obvious reduction in the secretion of either IL-4 or IL-5, nor by major changes in the IgG1 and IgE OVA-specific serum Ig profiles in the mutants. The markedly enhanced production of IFN-gamma in NOS2-/- mice was apparently responsible for the suppression of both eosinophilia and disease, as in vivo depletion of this factor restored allergic pathology in these animals. Our data indicate that NOS2 promotes allergic inflammation in airways via down-regulation of IFN-gamma activity and suggest that inhibitors of this molecule may represent a worthwhile therapeutic strategy for allergic diseases including asthma.
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PMID:Inhibition of allergic airway inflammation in mice lacking nitric oxide synthase 2. 988 18

The selective pulmonary vasodilatory effects of inhaled nitric oxide decrease pulmonary artery hypertension and improve arterial oxygenation in patients with ARDS without causing concomitant systemic vasodilation. Inhaled nitrix oxide therapy may decrease the prevalence of pulmonary edema, pulmonary barotrauma, and oxygen toxicity that occur with current ARDS treatment. The effect of nitric oxide on oxygenation and pulmonary artery pressure may allow more time for the lungs to recover. Initial results of clinical trials are encouraging; however, the impact of inhaled nitric oxide therapy on patients with ARDS remains unclear. Further research is needed to develop safe delivery systems and monitoring techniques for routine clinical use, to determine potential adverse and toxic effects of nitric oxide therapy on patients, and to determine the effects of long-term exposure to nitric oxide among healthcare workers. Concomitant administration of other medications with inhaled nitric oxide should also be investigated.
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PMID:Inhaled nitric oxide therapy for adult respiratory distress syndrome. 988 18

This study was undertaken to examine the combined effect of nitric oxide (NO) and hyperoxia on lung edema and Na,K-ATPase expression. Newborn piglets were exposed to room air (FiO2 = 0.21), room air plus 50 ppm NO, hyperoxia (FiO2 >/= 0.96) or to hyperoxia plus 50 ppm NO for 4-5 days. Animals exposed to NO in room air experienced only a slight decrease in Na,K-ATPase alpha subunit protein level. Hyperoxia, in the absence of NO, induced both the mRNA and the protein level of Na,K-ATP-ase alpha subunit and significantly increased wet lung weight, extravascular lung water, and alveolar permeability. NO in hyperoxia decreased the hyperoxic-mediated induction of Na,K-ATPase alpha subunit mRNA and protein while wet lung weight, extravascular lung water, and alveolar permeability remained elevated. These results suggest that 50 ppm of inhaled NO may not improve hyperoxic-induced lung injury and may interfere with the expression of Na,K-ATPase which constitutes a part of the cellular defense mechanism against oxygen toxicity.
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PMID:Influence of inhaled nitric oxide and hyperoxia on Na,K-ATPase expression and lung edema in newborn piglets. 992 7

The pathophysiology of exercise-induced hypoxaemia in elite athletes is still unclear but several studies indicate that a diffusion limitation, which could be explained by an interstitial pulmonary oedema, is a major contributing factor. Stress failure would induce a haemodynamical interstitial oedema with inflammatory reaction and release of mediators like histamine. Histamine release was found to be correlated with the hypoxaemia in elite athletes. If stress failure is involved, inhalation of pulmonary vasodilatators such as nitric oxide during exercise in athletes should induce an inhibition of the histamine release and a reversal of the hypoxaemia. Nine male endurance-trained young athletes performed two randomized exercise tests: one without and the other with 15 p.p.m. of inhaled NO. Measurements of histamine release and arterial blood gas analysis were performed at rest and at 50, 75 and 100% VO2max. At rest, inhaled NO induced a decrease in PaO2 and an increase in (Ai-a)DO2 suggesting increased perfusion of units with low V(A)/Q. During exercise, NO inhalation suppressed the histamine release observed without NO and induced a moderation in the decrease in PaO2 and the increase in (Ai-a)DO2 observed between 75 and 100% of VO2max (P < 0.005). In conclusion, this study showed that NO inhalation inhibited exercise-induced histamine release in highly trained athletes, but we were unable to confirm the suppression of exercise-induced hypoxaemia (EIH). An unexpected result was that inhaled NO seemed to have a marked effect on arterial oxygenation in highly trained-athletes, by disturbing gas exchanges.
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PMID:Effects of nitric oxide inhalation on pulmonary gas exchange during exercise in highly trained athletes. 1009 Mar 28

Nitric oxide (NO) may either protect against or contribute to inflammatory lung injury. In this study we investigated whether inhalation of 20 ppm NO alters tyrosine nitration, and we assessed the degree of lung inflammation and edema in rats after lipopolysaccharide (LPS) instillation. The amount of nitrotyrosine relative to the total amount of tyrosine was measured in lung homogenates, and lung tissue sections were stained for nitrotyrosine and aminotyrosine (a reduced form of nitrotyrosine). Leukocytes in bronchoalveolar lavage fluid (BALF) were counted, and myeloperoxidase activity was measured in lung homogenate. Lung edema and inflammatory cell accumulation in lung tissue were estimated by extravascular lung water weight (EVLW) and extravascular dry lung weight (EVDW), respectively. LPS instillation caused increases in nitrotyrosine concentration and immunohistochemical staining of nitrotyrosine and aminotyrosine in the lungs. LPS instillation increased the BALF leukocyte count, myeloperoxidase activity in lung tissue, and both EVLW and EVDW. Inhalational exposure to 20 ppm NO induced nitrotyrosine and aminotyrosine formation only in bronchial epithelial cell surface of the lungs not instilled with LPS. NO inhalation reduced the increases in nitrotyrosine and aminotyrosine in LPS-instilled lung tissue as well as the leukocyte count in BALF and myeloperoxidase activity in lung tissue, but it did not significantly change EVLW or EVDW. Leukocyte depletion in LPS-instilled rats reduced interstitial inflammatory cells, which were stained with nitrotyrosine and aminotyrosine, and attenuated the nitrotyrosine staining of alveolar capillaries. These results suggest that inhalation of 20 ppm NO reduces leukocyte accumulation in the lungs and inhibits tyrosine nitration caused by LPS instillation.
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PMID:Inhaled nitric oxide reduces tyrosine nitration after lipopolysaccharide instillation into lungs of rats. 1043 Jul 46


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