Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physiological and pathological respiratory responses are triggered by various conditions of exposure to cold climates. Beside airway smooth muscle, both the pulmonary and the tracheobronchial vasculatures are major effectors of respiratory responses to cold. General exposure to cold causes pulmonary vasoconstriction known as "Raynaud's phenomenon of the lung" in subjects with primary Raynaud syndrome and favors acute pulmonary oedema in subjects with congestive heart failure. In healthy subjects acute hyperventilation of very cold air has led to acute respiratory failure closely similar to hypoxic pulmonary oedema. In outdoor exercising people years long repetition of hyperventilation of subfreezing air causes "eskimo lung" made of obstructive lung disease and increased wall thickness of pulmonary arteries. At a lesser degree hyperventilation of dry air cools the central airways and triggers subclinical bronchial obstruction in healthy subjects. In asthmatic subjects hyperventilation of dry air causes asthma attacks. Results of recent animal and human experiments point to a key role of mucosal vessels in thermal balance of the airways. Simultaneously, there is increasing evidence that hyperventilation-induced asthma is triggered by a thermal stimulus.
 ...
PMID:Cold and the airways. 148 69

One hundred consecutive low birth weight (LBW) infants (less than 1751 g) were randomized into a study group having a restricted fluid intake until 4 weeks of age and a control group following the fluid regimen conventionally used in the hospital. Chest X-ray films were examined on admission, at the ages of 3 days, 7 days, 2 weeks and 4 weeks and at bi-monthly visits to the out-patient clinic up to 1 year of age or until the chest examinations were normal. The severity of hyaline membrane disease (HMD) and typical radiological abnormalities of bronchopulmonary dysplasia (BPD) were assessed. Twelve patients succumbed, 1 in the study group and 11 in the control group. The study group seemed to experience less severe HMD than the controls. Of the former 54% and 32% of the latter were alive and had no radiographical signs of BPD at 4 weeks of age (P less than 0.05). The difference between the groups in the cumulative number of normal chest X-ray examinations during the follow up was even more significant. The percentage of normal X-ray films at 1 year of age was 92% in the study group and 72% in the control group. These results suggest that fluid restriction for the first 4 weeks of life can lower the incidence of radiological abnormalities typical of BPD obtained during the 1st year of life in LBW infants. Pulmonary oedema seems to be a significant aetiological factor causing HMD to develop into chronic lung disease.
 ...
PMID:The relationship of fluid restriction during the 1st month of life to the occurrence and severity of bronchopulmonary dysplasia in low birth weight infants: a 1-year radiological follow up. 149 83

Industrialization of farming, animal raising, and forestry has added new chemical and mechanical hazards that need to be recognized and prevented. Lung disease among farm workers can result from a wide variety of hazardous exposures that include organic dusts, chemicals, and toxic gases. In addition to nonspecific symptoms of mucous membrane irritation, farm workers can develop occupational asthma or bronchitis, organic dust toxic syndrome, hypersensitivity pneumonitis, silo filler's disease (toxic hemorrhagic pulmonary edema), and neuromuscular respiratory failure.
 ...
PMID:Hazardous exposure and lung disease among farm workers. 151 56

In normal subjects, exercise widens the alveolar-arterial PO2 difference (P[A-a]O2) despite a more uniform topographic distribution of ventilation-perfusion (VA/Q) ratios. While part of the increase in P(A-a)O2 (especially during heavy exercise) is due to diffusion limitation, a considerable amount is caused by an increase in VA/Q mismatch as detected by the multiple inert gas elimination technique. Why this occurs is unknown, but circumstantial evidence suggests it may be related to interstitial pulmonary edema rather than to factors dependent on ventilation, airway gas mixing, airway muscle tone, or pulmonary vascular tone. In patients with lung disease, the gas exchange consequences of exercise are variable. Thus, arterial PO2 may increase, remain the same, or fall. In general, patients with advanced chronic obstructive pulmonary disease (COPD) or interstitial fibrosis who exercise show a fall in PO2. This is usually not due to worsening VA/Q relationships but mostly to the well-known fall in mixed venous PO2, which itself results from a relatively smaller increase in cardiac output than VO2. However, in interstitial fibrosis (but not COPD), there is good evidence that a part of the fall in PO2 on exercise is caused by alveolar-capillary diffusion limitation of O2 transport; in COPD (but not interstitial fibrosis), a frequent additional contributing factor to the hypoxemia of exercise is an inadequate ventilatory response, such that minute ventilation does not rise as much as does CO2 production or O2 uptake, causing arterial PCO2 to increase and PO2 to fall.
 ...
PMID:Ventilation-perfusion matching during exercise. 157 34

1. Research into the pathogenesis of acute and chronic neonatal lung disease has been hampered by the lack of a suitable small-animal model of prematurity. We describe such a model that has been developed and validated in the guinea-pig. 2. Pre-term guinea-pigs delivered by Caesarian section at 65 days gestation (normal gestation 68 days) exhibited transient respiratory distress. The survival of pre-term animals was lower than that of term animals after exposure to 95% O2 (pre-term 42% versus term 79% at 96 h, P less than 0.05). 3. Pulmonary histology in pre-term animals exposed to both 21% O2 and 95% O2 revealed evidence of acute lung injury with atelectasis, pulmonary oedema, fibrin deposition and inflammatory cell infiltration. No evidence of lung injury was observed in term animals exposed to 21% O2, whereas those exposed to 95% O2 showed a similar, but less pronounced, injury to that seen in pre-term pups. 4. The protein concentration in bronchoalveolar lavage fluid was similar in pre-term and term animals exposed to 95% O2, but neutrophil numbers in bronchoalveolar lavage fluid tended to be greater in pre-term pups. 5. Elastase-like activity, measured against succinyl-1-trialanine p-nitroanilide, was higher in bronchoalveolar lavage fluid from control pre-term animals compared with that from control term animals. Exposure to 95% O2 increased the elastase-like activity significantly in both groups. The majority of the elastase-like activity was EDTA-sensitive and thus is possibly due to metallo-elastase. Fractionation of bronchoalveolar lavage fluid indicated that the elastase-like activity was associated with a high-molecular-mass complex.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The pre-term guinea-pig: a model for the study of neonatal lung disease. 165 47

Cobalt, a metal with numerous industrial applications, has been associated with lung disease, an extreme form of which is an interstitial fibrosis. The biochemical mechanisms underlying this toxicity are not understood. In vitro studies have suggested that cobalt(II) ions are able to generate reactive oxidant species (possibly hydroxyl radical) in a reaction with hydrogen peroxide, and we have hypothesized that the occurrence of such an event in lung tissue, and the subsequent development of oxidative damage, may contribute to this pulmonary toxicity. The intratracheal instillation of CoCl2 into hamster lungs resulted after 3 h in decreased levels of reduced glutathione and increases in levels of oxidized glutathione and in the activity of the pentose phosphate pathway. These changes, which are compatible with the generation of oxidative stress, were reversed by 48 h at low Co2+ doses (1.0 to 1,000 micrograms/kg). Irreversible changes at higher doses coincided with the onset of pulmonary edema. Incubation of lung slices with CoCl2 (0.1 to 10 mM) resulted in time- and Co2+ concentration-dependent increases in levels of oxidized glutathione and protein-mixed disulfides and a decrease in reduced glutathione. A concentration-dependent stimulation of the pentose phosphate pathway was also observed. These changes preceded the detection of overt cell toxicity, as assessed by various biochemical parameters. These data indicate that thiol oxidation constitutes an early event in the pulmonary toxicity of cobalt(II) ions and are compatible with the hypothesis that the generation of oxidative stress may be of significance to the toxic process.
 ...
PMID:Indices of oxidative stress in hamster lung following exposure to cobalt(II) ions: in vivo and in vitro studies. 189 47

Drug-induced lung disease presents several diagnostic and therapeutic problems to the clinician. This is especially true in the case of lung disease associated with antirheumatic agents in which pulmonary disease may be due to the underlying disorder. Unfortunately, no specific markers exist to differentiate drug-induced lung disease from other pathologic processes. In addition, the numerous drugs often used simultaneously or in close sequence in rheumatic disorders make assignment of toxicity to a specific agent difficult. Six groups of drugs used as anti-inflammatory/antirheumatic agents have been discussed in association with pulmonary damage penicillamine, gold, methotrexate, salicylates, NSAIDs, and colchicine. The major clinical syndromes ascribed to these drugs include hypersensitivity pneumonitis and chronic alveolitis/fibrosis (penicillamine, gold, methotrexate, NSAIDs), pulmonary-renal syndrome (penicillamine), bronchiolitis obliterans (penicillamine, gold), and noncardiogenic pulmonary edema (salicylates, colchicine). Unfortunately, treatment options remain limited. Withdrawal of the offending drug and supportive care are the mainstays of therapy. In cases in which active inflammation causes significant derangement of gas exchange, corticosteroids are warranted. More aggressive management using immunosuppressive drugs has been recommended in cases of refractory PABO and PAGS, but these recommendations are at present based only on isolated case reports.
 ...
PMID:Pulmonary disease due to antirheumatic agents. 196 88

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
 ...
PMID:Metal toxicity and the respiratory tract. 217 66

The effects of "hypocirculation" and "hypercirculation" of the lungs are small. Hypocirculation has an influence of the ventilation/perfusion ratio, and can thus contribute to hypocapnia. In the early stages, hypercirculation--in particular via a left-to-right shung, leads to an increase in diffusion capacity; after a course of many years, a "counter-situation" occurs. Progressive pulmonary hypertension, as is exemplified for mitral stenosis, leads to measurable restrictive and obstructive impairment of function, and possible to unspecific hyper-reaction, as also, over the long-term, to a diminishement in membrane diffusion capacity. Chronic left heart failure is characterised by interstitial oedema at the level of the alveolar and bronchial capillary beds. The results are measurable restrictions in the static volumes, and in particular of the obstruction parameters and the closing volume that involve the small airways. In the individual case, no statement as to the extent of left heart failure is possible. In the passive pulmonary hypertension phase, diffusion capacity increases; in the further course of the disease, with development of interstitial and alveolar oedema, it decreases again. In acute left heart failure, the persistance and/or extent of pulmonary oedema is not determined solely by the magnitude of the pulmonary venous pressure. Permeability oedema--brought about by mediators--would appear to be significant on the basis of animal experiments. Not infrequently, left cardiac failure leads to small pleural effusions which occur in combination with substantial atelectasia, the aetiology of which is unclear. Interpretation difficulties are caused by the clinical findings and function-analytical data obtained in patients with a combination of chronic lung disease and reducted volume storage capacity of the pulmonary circulation and of the left heart failure, a common situation in the elderly patient. Diminished pulmonary function parameters that fail to adequate respond to bronchodilators may be an expression of left ventricular failure.
 ...
PMID:[The lung in heart diseases]. 219 2

Magnetic resonance imaging (MRI) is considered inferior to computed tomography (CT) in the assessment of lung parenchyma, being hampered by low proton density, magnetic susceptibility effects, flow, and cardiac and respiratory motion. In this study the authors assessed the potential usefulness of MRI by comparing it with corresponding CT images of the lung in the absence of motion. They studied eight excised normal canine lung lobes inflated with oxygen before and after induction of pulmonary edema produced by intravascular infusion of saline at 30 cm H2O. T1, T2 and proton density weighted, 5-mm thick, gapped, multislice sequences were performed at 1.5 T. Magnetic resonance images were compared with corresponding 5-mm collimation CT scans at identical levels both before and after the induction of pulmonary edema. The MR and CT scans were assessed independently by two chest radiologists. In normal lung, there was equivalent visualization of vessels down to 1 mm and bronchi to 2 mm in diameter. T1 and proton density scans demonstrated lower spatial resolution but greater contrast than the corresponding CT images. In pulmonary edema both T1 and proton density sequences demonstrated peribronchial edema with greater contrast than CT. Air-space filling was equally well demonstrated by either technique. The authors conclude that, in motionless lung, MRI has lower spatial but greater contrast resolution than CT. It is potentially superior to CT in assessing focal and diffuse lung disease if cardiac and respiratory motion artifacts can be minimized or suppressed.
 ...
PMID:Magnetic resonance imaging of hydrostatic pulmonary edema in isolated dog lungs: comparison with computed tomography. 220 89


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>