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)

Hyperpermeability is a crux of pathogenesis of sudden lung edema in many pulmonary disorders, especially in acute lung injury and adult respiratory distress syndrome (ARDS). Using our modified method for assessment of pulmonary vascular permeability, we observed the effects of xanthine with xanthine oxidase (X-XO) perfused in rat pulmonary artery and the protection of vasoactive intestinal polypeptide (VIP) against the injury of pulmonary vascular permeability. After addition of xanthine oxidase in the perfusate reservoir containing xanthine, 125I-albumin leak index (125IALI) was remarkably increased while peak airway pressure (Paw) was not significantly increased, and perfusion pressure of pulmonary artery (Ppa) and lung wet/dry weight ratio (W/D) were only slightly increased. Xanthine plus xanthine oxidase also increased thromboxane B2 (TX B2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in the perfusate. Treatment with VIP obviously reduced or totally prevented all signs of injury. Simultaneously, VIP also diminished or abolished the associated generation of arachidonate products. The results indicated that VIP has potent protective activity against injury of pulmonary vascular permeability and may be a physiological modulator of inflammatory damage to vascular endothelium associated with toxic oxygen metabolites.
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PMID:Vasoactive intestinal polypeptide prevents injury of pulmonary vascular permeability due to xanthine with xanthine oxidase. 858 Apr 82

Re-expansion pulmonary oedema is a recognised but rare complication following the rapid drainage of a large pleural effusion or pneumothorax [1,2], usually occurring on the side of re-inflation. The pathogenesis of the pulmonary oedema is poorly understood but is thought to be due to micro-vascular shearing resulting in neutrophil activation and adhesion to the vascular endothelium resulting in increased micro-vascular permeability [3-7]. Few reports appear in the literature of invasive haemodynamic monitoring following this catastrophe. We describe a patient who sustained fatal pulmonary oedema arising in the contralateral lung, with pulmonary flow catheter data documenting the initial circulatory collapse following the aspiration of a massive pulmonary effusion.
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PMID:Catastrophic circulatory collapse following re-expansion pulmonary oedema. 878 12

Anti-CD7-dgA, DA7, consists of deglycosylated ricin A chain coupled to a mouse monoclonal anti-human CD7 antibody. This study determined the maximally tolerated dose (MTD) of this immunotoxin administered as a one hour infusion over five days to 11 patients with T-cell lymphoma (>30% CD7+ malignant cells). The MTD was 0.2 mg/kg/day or 1 mg/kg/120 hours (maximal toxicity grade 3) with vascular leak syndrome (VLS) as dose-limiting toxicity (DLT). Predictors of severe VLS included age and absence of circulating lymphoma cells. Two partial responses and one minimal response were seen. Patients with minimal lymphoma burden or T-cell large granular lymphocyte (LGL) leukemia showed the best responses. The mean maximal serum concentration of immunotoxin at the MTD was 2.5 ug/ml. The mean alpha-phase half-life was 1.5 hours and the mean beta-phase half-life was 8 hours. Repeated dosing had minimal effects on either peak serum immunotoxin concentrations or serum half-lives. While human antimouse antibodies were observed, they were low in concentration (<55 ng/ml). Human anti-ricin antibody was elevated in one patient (190 ng/ml). VLS presented with hypoalbuminemia, dyspnea, pulmonary edema, aphasia, and peripheral edema and cleared over a two week period. Serum fibronectin levels were measured in three patients and were very low in one patient who developed VLS. No specific binding of DA7 immunotoxin was seen with vascular endothelium in various human tissues.
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PMID:Therapy of patients with T-cell lymphomas and leukemias using an anti-CD7 monoclonal antibody-ricin A chain immunotoxin. 932 91

Genes of an influenza A (H5N1) virus from a human in Hong Kong isolated in May 1997 were sequenced and found to be all avian-like (K. Subbarao et al., Science 279:393-395, 1998). Gene sequences of this human isolate were compared to those of a highly pathogenic chicken H5N1 influenza virus isolated from Hong Kong in April 1997. Sequence comparisons of all eight RNA segments from the two viruses show greater than 99% sequence identity between them. However, neither isolate's gene sequence was closely (>95% sequence identity) related to any other gene sequences found in the GenBank database. Phylogenetic analysis demonstrated that the nucleotide sequences of at least four of the eight RNA segments clustered with Eurasian origin avian influenza viruses. The hemagglutinin gene phylogenetic analysis also included the sequences from an additional three human and two chicken H5N1 virus isolates from Hong Kong, and the isolates separated into two closely related groups. However, no single amino acid change separated the chicken origin and human origin isolates, but they all contained multiple basic amino acids at the hemagglutinin cleavage site, which is associated with a highly pathogenic phenotype in poultry. In experimental intravenous inoculation studies with chickens, all seven viruses were highly pathogenic, killing most birds within 24 h. All infected chickens had virtually identical pathologic lesions, including moderate to severe diffuse edema and interstitial pneumonitis. Viral nucleoprotein was most frequently demonstrated in vascular endothelium, macrophages, heterophils, and cardiac myocytes. Asphyxiation from pulmonary edema and generalized cardiovascular collapse were the most likely pathogenic mechanisms responsible for illness and death. In summary, a small number of changes in hemagglutinin gene sequences defined two closely related subgroups, with both subgroups having human and chicken members, among the seven viruses examined from Hong Kong, and all seven viruses were highly pathogenic in chickens and caused similar lesions in experimental inoculations.
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PMID:Comparisons of highly virulent H5N1 influenza A viruses isolated from humans and chickens from Hong Kong. 965 15

The effects of long-term preoperative administration of low-dose erythromycin (EM) were experimentally examined in relation to the treatment of reperfusion disorders following pulmonary thermal ischemia. EM was administered at a dose of 100 mg/day for 1 month to adult mongrel dogs with an average weight of about 12 kg (EM group). A control group that did not receive EM was also enrolled. Using a pulmonary autograft model, collapse-thermal ischemia of the lungs was performed on each animal for 60 minutes. In the early stage of reperfusion, the following measurements were assessed: gas-exchange potency in the left lung, hemodynamics, water content, adhesion of neutrophils to vascular endothelium, and concentration of blood eicosanoids. The results for the 2 groups were then compared. In the control group, the blood level of leukotriene B4 (LTB4) increased shortly after reperfusion, neutrophils migrated toward the vascular endothelium and adhered to it, and pulmonary edema developed after 1 hour. However in the EM group, the blood level of thromboxane B2 was significantly suppressed before and after hilar stripping, and the increase in the blood LTB4 level and the migration of neutrophils shortly after reperfusion in thermal ischemia were suppressed. Eventually alleviation of pulmonary edema was indicated and significantly improved gas exchange was maintained. In conclusion, pulmonary injury during detachment of the hilum of the lung, as well as warm ischemia-reperfusion pulmonary injury, may be alleviated by preoperative administration of low-dose EM on a long-term basis.
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PMID:[Effects of long-term preoperative administration of low-dose erythromycin on warm ischemia-reperfusion pulmonary injury]. 991 77

Inflammatory reactions are associated with sequestration of leukocytes in the lung. Complement activation leads to accumulation of leukocytes in alveolar septa and alveoli, to lung edema and hemorrhage. Although in organs other than the lung leukocytes interact with the vascular endothelium only in postcapillary venules, alveolar capillaries are considered to be the site of leukocyte sequestration in the lung. However, pulmonary venules and arterioles have not been investigated systematically after complement activation so far. A closed thoracic window was implanted in anesthetized rabbits; leukocytes and red blood cells were stained, and the movement of these cells was measured in superficial pulmonary arterioles, venules and alveolar capillaries using fluorescence video microscopy before and 30 and 60 min after infusion of cobra venom factor (CVF). Erythrocyte velocity and macrohemodynamic conditions did not change after CVF infusion and were not different from the sham-treated controls. The number of sticking leukocytes increased significantly compared to baseline and control: by 150% in arterioles and in venules and by 740% in alveolar capillaries within 60 min after CVF infusion. The width of alveolar septa in vivo was significantly enlarged after CVF infusion, indicating interstitial pulmonary edema. At the end of the experiments, myeloperoxidase activity was higher in the CVF group, showing leukocyte sequestration in the whole organ. It is concluded that complement activation by CVF induces leukocyte sequestration in lung arterioles, venules and alveolar capillaries and leads to mild lung injury.
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PMID:Leukocyte sequestration in pulmonary microvessels and lung injury following systemic complement activation in rabbits. 1047 42

Acute chest syndrome (ACS) is characterized by chest pain with dyspnea and recent radiologic abnormalities, and is an acute lung complication whose problem is one of etiology. Alveolar hypoventilation linked to infarcts of the thoracic ribs, thoracoabdominal trauma, subdiaphragmatic pain, the administration of analgesics causing respiratory depression, or sleep disturbance, is a frequent cause of ACS. Bronchoalveolar lavage has revealed the frequency of fat embolism following infarcts in the long bones. Pulmonary vascular occlusion, due to thrombosis or emboli, is rare, as are the infectious pneumonia and pulmonary edema. The pathogenetic mechanisms consist of an alteration of the rheological properties of the blood, the existence of an hypercoagulability state, specific interactions between the abnormal sickle cells and the vascular endothelium, and a dysregulation of the vascular reactivity. Research centered around NO biology has led to an expanded understanding of the critical interdependence of NO, hemoglobin, and the microvasculature. An anemic patient with ACS suffers from loss of pulmonary scavenging and hypoxic pulmonary vasoconstriction and loss of peripheral NO delivery. Interruption of this cycle by transfusing normal (hemoglobin A-containing) erythrocytes might improve all the abnormalities.
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PMID:[Respiratory distress and drepanocytosis]. 1079 55

Direct bird-to-human transmission, with the production of severe respiratory disease and human mortality, is unique to the Hong Kong-origin H5N1 highly pathogenic avian influenza (HPAI) virus, which was originally isolated from a disease outbreak in chickens. The pathobiology of the A/chicken/Hong Kong/220/97 (H5N1) (HK/220) HPAI virus was investigated in chickens, turkeys, Japanese and Bobwhite quail, guinea fowl, pheasants, and partridges, where it produced 75-100% mortality within 10 days. Depression, mucoid diarrhea, and neurologic dysfunction were common clinical manifestations of disease. Grossly, the most severe and consistent lesions included splenomegaly, pulmonary edema and congestion, and hemorrhages in enteric lymphoid areas, on serosal surfaces, and in skeletal muscle. Histologic lesions were observed in multiple organs and were characterized by exudation, hemorrhage, necrosis, inflammation, or a combination of these features. The lung, heart, brain, spleen, and adrenal glands were the most consistently affected, and viral antigen was most often detected by immunohistochemistry in the parenchyma of these organs. The pathogenesis of infection with the HK/220 HPAI virus in these species was twofold. Early mortality occurring at 1-2 days postinoculation (DPI) corresponded to severe pulmonary edema and congestion and virus localization within the vascular endothelium. Mortality occurring after 2 DPI was related to systemic biochemical imbalance, multiorgan failure, or a combination of these factors. The pathobiologic features were analogous to those experimentally induced with other HPAI viruses in domestic poultry.
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PMID:Pathobiology of A/chicken/Hong Kong/220/97 (H5N1) avian influenza virus in seven gallinaceous species. 1128 Mar 71

Exposure to Cd(2+) via inhalation or intratracheal instillation results in pulmonary edema, which is followed by the influx of leukocytes, the proliferation of type II pneumocytes and eventual scarring and fibrotic changes. While the general toxic effects of Cd(2+) in the lung have been well characterized, the specific molecular mechanisms underlying these effects have yet to be elucidated. Previously we have shown that Cd(2+) can disrupt the adhering junctions between various types of epithelial and endothelial cells in culture, most likely by perturbing the function of the Ca(2+) dependent cell adhesion molecules E-cadherin and VE-cadherin respectively. The objectives of this study were to determine whether respiratory exposure to Cd(2+) can alter the localization of E-cadherin and VE-cadherin in the lung, and to determine whether this effect may play a role in the acute pneumotoxic response to Cd(2+). Male CF-1 mice were exposed to CdCl(2) (0, 16.25, 32.5, 65 or 130 nmoles in 50 microl saline) via intratracheal instillation. After 24 hours, the lungs were removed and either subjected to bronchoalveolar lavage or analyzed for histopathologic changes. The results showed that Cd(2+) caused an increase in lung weight and in the protein content of the lavage fluid. These effects were accompanied by a pronounced decrease in the amount of E-cadherin in epithelial cells of the alveoli and small bronchioles and of VE-cadherin in vascular endothelial cells. Assessment of cell membrane integrity with ethidium homodimer-1 showed no evidence of severe injury or death in alveolar epithelial cells. These findings suggest that E-cadherin and VE-cadherin may be important early targets of Cd(2+) toxicity in the lung.
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PMID:Effects of cadmium on E-cadherin and VE-cadherin in mouse lung. 1257 Sep 30

(1) Intravenous injection of ioxaglate (4 g iodine kg(-1)), an iodinated radiographic contrast medium, caused a marked protein extravasation, pulmonary oedema and a decrease in the arterial partial oxygen pressure in rats. (2) All of these reactions to ioxaglate were reversed by the pretreatment with gabexate mesilate (10 and 50 mg kg(-1), 5 min prior to injection) or nafamostat mesilate (3 and 10 mg kg(-1)), in which the inhibition was complete after injection of nafamostat mesilate (10 mg kg(-1)). (3) Both gabexate mesilate and nafamostat mesilate inhibited the activity of purified human lung tryptase, although the latter compound was far more potent than the former. (4) Ioxaglate enhanced the nafamostat-sensitive protease activity in the extracellular fluid of rat peritoneal mast cell suspensions. (5) Tryptase enhanced the permeability of protein through the monolayer of cultured human pulmonary arterial endothelial cells. Ioxaglate, when applied in combination with rat peritoneal mast cells, also produced the endothelial barrier dysfunction. These effects of tryptase and ioxaglate were reversed by nafamostat mesilate. (6) Consistent with these findings, immunofluorescence morphological analysis revealed that tryptase or ioxaglate in combination with mast cells increased actin stress fibre formation while decreasing VE-cadherin immunoreactivity. Both of these actions of tryptase and ioxaglate were reversed by nafamostat mesilate. (7) These findings suggest that tryptase liberated from mast cells plays a crucial role in the ioxaglate-induced pulmonary dysfunction. In this respect, nafamostat mesilate may become a useful agent for the cure or prevention of severe adverse reactions to radiographic contrast media.
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PMID:A potent tryptase inhibitor nafamostat mesilate dramatically suppressed pulmonary dysfunction induced in rats by a radiographic contrast medium. 1264 98


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