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)

A 33 years old woman was admitted to the hospital after four days with cough, dyspnea, orthopnea and hemoptysis. Blood pressure was 170/90 mmHg, pulse was 112 and temperature was normal. She had cyanosis and a left ventricular gallop, without heart murmurs. A chest radiograph revealed pulmonary edema and echocardiogram showed a global left ventricular systolic disfunction. Oxygen and furosemide were started, but cardiopulmonary collapse ensued. The patient was supported with mechanical ventilation and treated with inotropic drugs. A right sided cardiac catheterization showed pulmonary wedge pressure of 18 mmHg and a cardiac index of 3 l/min/m2. The levels of creatinine and urea nitrogen were elevated and a urine protein was 97 mg/dl. Coagulation tests were normal except by a positive lupic anticoagulant. Markers of connective tissue diseases or vasculitis were negatives. The clinical evolution suggested that a catastrophic antiphospholipid syndrome was ongoing. Intravenous corticoids, gammaglobulin and cyclophosphamide were administered with transient improvement. On her fourth day of treatment, the patient presented sudden pulmonary bleeding and embolism. A plasmapheresis was performed with improvement of renal, cardiac and pulmonary function. After this episode, the patient has been treated with prednisone and oral anticoagulants treatment for the last two years, without further clinical events.
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PMID:[Catastrophic antiphospholipid syndrome and acute heart failure. Report of a case]. 1463 91

Reactive oxygen and nitrogen species have been implicated in the pathogenesis of pulmonary diseases. The goal of this study was to measure the response of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 enzymes (COX-2) in lung with moderate zinc deficiency. Adult male Wistar rats were divided into two groups receiving (1) a zinc-deficient diet (ZD) or (2) a zinc-adequate control diet. After 2 months of treatment, the zinc-deficient group showed a significant pulmonary edema. This was associated to a reduction of protein thiols and to a significant increase of metallothionein and glutathione disulfide levels. In addition, a higher serum and lung NO production in ZD group was positively related to the higher activity and expression of iNOS and COX-2 found in lungs. Western blot analysis revealed increased IkappaBalpha degradation, an indicator of NF-kappaB activation in ZD lungs. Anatomopathologic analysis of ZD lungs showed an increase of connective tissue fibers with an influx of polymorphonuclear cells. These cells and type II cells from the alveoli showed specific immunohistochemical signals for iNOS. The conclusion is that, during the development of zinc-deficiency, iNOS activity increases in lung and contributes to lung injury. Zinc deficiency implications must be taken into account to design therapies and public health interventions involving targeted zinc supplementation for high-risk subjects or certain diseases, such as asthma.
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PMID:Overexpression of inducible nitric oxide synthase and cyclooxygenase-2 in rat zinc-deficient lung: Involvement of a NF-kappaB dependent pathway. 1625 82

We investigated the effects of normobaric hypoxia on rat lungs and hypothesized that the hypoxic exposure would induce lung injury with pulmonary edema and inflammation ensued by development of fibrosis. Rats were exposed to 10% O(2) in nitrogen over 6-168h. We analyzed cardiovascular function and pulmonary changes, lung histology and mRNA expression of extracellular matrix (ECM) molecules in the lung. Significant hemodynamic changes occurred after 168h of hypoxic exposure. Moderate pulmonary edema appeared after 8h and peaked after 16h of hypoxia. It was accompanied by inflammation, fibrosis and vascular hypertrophy. mRNA expression of transforming growth factor-beta2 and -beta3 was up-regulated in lung tissue after 8h of hypoxia. After 8-16h, mRNA expression of collagen types I and III and of other ECM molecules was significantly elevated and increased further with longer exposure to hypoxia. The time course of hypoxia-induced pulmonary injury resembled that previously observed after continuous norepinephrine infusion in rats.
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PMID:Time course of hypoxia-induced lung injury in rats. 1759 12

Toxic silo gases are a potential danger to livestock housed in close proximity to roughage silos. These gases, such as nitrogen dioxide (NO2), may be produced during the early stages of (maize and grass) silage making. In humans, inhalation of these gases causes a condition known as 'Silo Filler's Disease' (SFD), which is a recognized occupational hazard for workers in upright forage silos in many countries. NO2 accumulates on top of silage, is inhaled by workers, and reacts with water on the airway surfaces to form nitrous acid, which damages the lung and causes pulmonary oedema, bronchiolitis, and death in severe cases. On a dairy farm, a cloud of reddish-brown NO2 gas (which is heavier than air) was noticed to escape from underneath the plastic sheet of a horizontal maize bunker and to enter a cubicle house for dairy cows 1 day after ensiling. Eleven cows became dyspnoeic, 3 of which subsequently died. A combination of weather conditions, an insufficient sand load on the maize bunker, the utilization of a lactobacillus starter culture, and the close proximity of the silo to the cubicle house may have caused the incident.
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PMID:Nitrogen dioxide (silo gas) poisoning in dairy cattle. 1799 Jun 32

During and after surgical procedures, there is a well defined physiological stress response that involves activation of inflammatory, endocrine, metabolic, and immunological mediators. Oxidative stress, which is defined to be a situation where the production of reactive oxygen/nitrogen species exceeds the mechanisms required to detoxify them, is believed to be an integrated part of the surgical stress response. Oxidative stress per se may be associated with complications such as myocardial injury, sepsis, pulmonary edema, kidney and liver failure, and increased mortality. Melatonin is a potent antioxidant and in many studies melatonin has been shown to be more effective than some "classical" antioxidants (e.g., vitamins E and C) in protecting against oxidative/nitrosative stress. There are numerous experimental studies in which the antioxidant properties of melatonin have been proven. In preliminary studies in newborns with asphyxia, sepsis, or respiratory distress syndrome, melatonin has proven to be a highly potent antioxidant. This review summarizes the results of animal and human studies wherein melatonin was shown to modulate oxidative stress; this discussion emphasizes the stress response related to surgery.
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PMID:Oxidative stress in relation to surgery: is there a role for the antioxidant melatonin? 1826 62

Although reexpansion of a collapsed lung often causes pulmonary edema, the pathogenesis of the condition is not yet fully understood. To determine whether inflammatory changes occur in the pulmonary circulation during atelectasis and study the mechanism underlying the development of reexpansion pulmonary edema, we used a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 1 h. We evaluated the accumulation of polymorphonuclear leukocytes (PMNs) in the lung and the production of reactive oxygen species (ROS) in the pulmonary circulation using a fluorescent imaging technique. We also used confocal laser scanning microscopy and computerized image analysis to evaluate the membrane translocation of p47-phox, one of the nicotinamide adenine dinucleotide phosphate (reduced form) oxidase subunits, in PMNs sequestered in the lung. Polymorphonuclear leukocytes accumulated in the lung during atelectasis, and p47-phox was translocated to the plasma membrane, but no ROS production was observed. Marked PMN ROS production was observed after reexpansion of the collapsed lung with air. Little ROS production was observed when the lung was reexpanded with nitrogen. During atelectasis, PMNs accumulate in the lung, where they are primed for respiratory bursting. After pulmonary reexpansion, oxygen is supplied from the alveoli, and PMN respiratory bursting occurs.
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PMID:Polymorphonuclear leukocytes are activated during atelectasis before lung reexpansion in rat. 1856 28

Severe uremia is now a rare occurrence in most developed nations, and yet is still present in many countries of the world. It includes clinical manifestations such as calciphylaxis and uremic frost, which are now rarely seen. Patients with extremely high levels of blood urea nitrogen (above 175 mg/dL) are at a higher risk of experiencing first-time hemodialysis-related complications, in particular dialysis disequilibrium syndrome (DDS). DDS is a central nervous disorder characterized by a wide variety of neurological symptoms that range from nausea and vomiting to even death due to cerebral edema. There are 2 main theories to explain its pathophysiology: the reverse urea effect, which considers that the shift of urea between brain intracellular space and plasma is not immediate, causing a higher concentration of urea within the brain and leading to cerebral edema. The second theory considers that after hemodialysis, patients have transient paradoxical metabolic acidosis within the central nervous system, displacing Na(+) and K(+) from organic anions, making them osmotically active and again leading to cerebral edema. The main goal is to prevent the occurrence of DDS, for which there are several proposed measures including continuous renal replacement therapies. Once established, treatment should be focused on supportive therapy. Another uncommon phenomenon described in patients who initiate hemodialysis is transient pulmonary leukocyte margination, which in conjunction with an inflammatory milieu, may lead to non-cardiogenic pulmonary edema. We present the case of a young adult with severe uremia who, despite application of recommended measures, developed DDS and non-cardiogenic pulmonary edema.
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PMID:Dialysis disequilibrium syndrome and other treatment complications of extreme uremia: a rare occurrence yet not vanished. 1863 82

This is a brief overview of physiological reactions, limitations, and pathophysiological mechanisms associated with human breath-hold diving. Breath-hold duration and ability to withstand compression at depth are the two main challenges that have been overcome to an amazing degree as evidenced by the current world records in breath-hold duration at 10:12 min and depth of 214 m. The quest for even further performance enhancements continues among competitive breath-hold divers, even if absolute physiological limits are being approached as indicated by findings of pulmonary edema and alveolar hemorrhage postdive. However, a remarkable, and so far poorly understood, variation in individual disposition for such problems exists. Mortality connected with breath-hold diving is primarily concentrated to less well-trained recreational divers and competitive spearfishermen who fall victim to hypoxia. Particularly vulnerable are probably also individuals with preexisting cardiac problems and possibly, essentially healthy divers who may have suffered severe alternobaric vertigo as a complication to inadequate pressure equilibration of the middle ears. The specific topics discussed include the diving response and its expression by the cardiovascular system, which exhibits hypertension, bradycardia, oxygen conservation, arrhythmias, and contraction of the spleen. The respiratory system is challenged by compression of the lungs with barotrauma of descent, intrapulmonary hemorrhage, edema, and the effects of glossopharyngeal insufflation and exsufflation. Various mechanisms associated with hypoxia and loss of consciousness are discussed, including hyperventilation, ascent blackout, fasting, and excessive postexercise O(2) consumption. The potential for high nitrogen pressure in the lungs to cause decompression sickness and N(2) narcosis is also illuminated.
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PMID:The physiology and pathophysiology of human breath-hold diving. 1897 67

The pathogenesis of lung injury by exposure to highly toxic sulfur and nitrogen mustards involves alkylating damage of the respiratory epithelium followed by an acute inflammatory response and lung edema. The acute phase is followed by long-term respiratory complications characterized by bronchitis, lung fibrosis, and airway hyperreactivity. In this study, we utilized a mouse model for airway inflammation induced by inhalation exposure to the alkylating nitrogen mustard melphalan, in order to investigate possible beneficial treatment effects by the corticosteroid dexamethasone. In addition, we investigated therapeutic efficacy of liposome-encapsuled vitamin E, an antioxidant formulation previously shown to be efficient in counteracting inflammatory conditions. Influx of inflammatory cells to airways, edema formation, and expression of different cytokines were analyzed 6 and 18 hours after exposure to melphalan. In order to evaluate long-term lung effects, we also investigated collagen deposition and accumulation of lymphocytes at 2 and 4 weeks after exposure. A single intraperitoneal injection of dexamethasone (10 mg/kg body weight) 1 hour after melphalan exposure significantly reduced interleukin (IL)-1 and IL-6 in bronchoalveolar lavage fluid (BALF) and diminished the acute airway inflammation. Our results also indicate that early single-dose treatment with dexamethasone protects against long-term effects observed 2-4 weeks after melphalan exposure, as indicated by reduced lymphocytic response in airways and decreased collagen deposition. Furthermore, our results indicate that also vitamin E (50 mg/kg) reduces acute inflammatory cell influx, and suppresses collagen formation in lung tissue, indicating that this drug could be used in combination with corticosteroids for protection against chemical-induced lung injury.
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PMID:Treatment with dexamethasone or liposome-encapsuled vitamin E provides beneficial effects after chemical-induced lung injury. 1957 81

Indole and 3-methylindole (skatole) are odor pollutants in livestock waste, and skatole is a major component of boar taint. Skatole causes pulmonary edema and emphysema in ruminants and causes damage to lung Clara cells in animals and humans. A gas chromatographic method that originally used a nitrogen-phosphorus detector to increase sensitivity was modified resulting in an improved flame ionization detection response for indole and skatole of 236% and 207%, respectively. The improved method eliminates the large amount of indole decomposition in the injector. A 10 micro g mL(-1) spike of indole and skatole in water and swine fecal slurries resulted in recovery of 78.5% and 96% in water and 76.1% and 85.8% in fecal slurries, respectively. The effect of the addition of nitroethane and nitroethanol at 21.8 mM in swine fecal slurries was studied on the microbial production of indole and skatole. Nitroethane and nitroethanol decreased the production of skatole in swine fecal slurries at 24 h. The nitroethane effect on l-tryptophan-supplemented fecal slurries after 6 and 24 h incubation resulted in a decrease of 69.0% (P = 0.02) and 23.5% skatole production, respectively, and a decrease of 14.9% indole at 6 h, but an increase in indole production of 81.1% at 24 h.
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PMID:Effect of nitroethane and nitroethanol on the production of indole and 3-methylindole (skatole) from bacteria in swine feces by gas chromatography. 2018 70


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