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

In pulmonary edema, fluid accumulates first in the interstitium, then in the alveoli. However, the relative amounts of interstitial fluid around arteries and veins of different sizes are unknown; in addition, the effects of fixation on the light microscopic quantitation of edema are unclear. To answer these questions, we induced permeability pulmonary edema in seven anesthetized dogs with 27 mg/kg of alpha-naphthylthiourea. Pulmonary artery and wedge pressures were measured. After moderately severe edema, diagnosed by chest x-ray and falling arterial pO2, lobes were fixed by airways instillation or vascular perfusion with glutaraldehyde and formaldehyde or were frozen with liquid nitrogen. With light microscopy, the edema surrounding arteries and veins of different sizes was measured using a computer equipped with a digitizing tablet and expressed as the edema ratio = area of perivascular edema/area of vessel, or as an absolute area of edema. Alveolar edema was graded semiquantitatively, and wet weight to dry weight ratios were calculated. Two control dogs were also studied. During the induction of edema, pulmonary artery and wedge pressures did not change significantly. Mean wet weight to dry weight ratios were 9.3 +/- 1.1. We found that the edema ratio was greater (p less than 0.01) for arteries (2.75, n = 1305) than for veins (1.40, n = 900). The edema ratio was greater for vessels more than 400 micron than less than 400 micron (p less than 0.01) and greater in the instillation- and perfusion-fixed lobes than in the frozen lobes (p less than 0.01). Similar results were obtained for the absolute areas of periarterial and perivenous edema. Less alveolar edema was seen in the lobes fixed by instillation (p less than 0.01). We conclude that, in permeability edema induced by alpha-naphthylthiourea, the fluid accumulates preferentially around arteries compared with veins and around larger compared with smaller vessels. Airways instillation and vascular perfusion fixation appeared to increase interstitial fluid cuffs compared to freezing.
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PMID:Quantitative morphology of permeability lung edema in dogs induced by alpha-naphthylthiourea. 641 82

The thermal-green dye indicator dilution method for measuring extravascular lung water (EVLW) has been extensively validated against gravimetric EVLW, but no reports to date have correlated in vivo EVLW with pulmonary physiologic parameters or postmortem lung morphologic findings. A predetermined level of hydrostatic edema was created in 12 swine by the variable inflation of a left atrial Foley balloon. EVLW, arterial and mixed venous blood gases, and mixed expired gases were before balloon inflation and periodically throughout the experiment. The animals were killed by rapid excision of the lungs, which were then reinflated and frozen in liquid nitrogen. Postmortem morphometrics were performed by photographing random sections of the lungs while still frozen. A blinded observer measured perivascular cuff width, interlobular septal width, and percent of alveoli flooded on each section. Perivascular cuff width:vessel diameter ratio correlated linearly with EVLW (r2 = 0.76; p less than 0.0001) and increased 25% for each 5 ml/kg of EVLW. Alveolar flooding did not begin until EVLW had doubled from normal to 11.4 ml/kg but then increased linearly with EVLW, reaching 60% flooding at 21 ml/kg. Increase in shunt fraction correlated linearly with increases in EVLW (r2 = 0.76; p less than 0.001) and increased approximately 10% for each EVLW increment of 5.0 ml/kg. We conclude that in vivo EVLW measurements correspond closely to more conventional morphologic and physiologic measurements and sensitively detect all levels of pulmonary edema from minimal perivascular cuffing to fulminant alveolar flooding.
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PMID:Morphologic and physiologic correlates of increased extravascular lung water. 646 67

Changes in blood volume were investigated following intravenous injection of a single dose of furosemide in 21 patients with pulmonary edema. In a subset of 10 patients in whom the blood urea nitrogen level was 11.4 +/- 2.2 mg/dl and the serum creatinine level was 1.3 +/- 0.1 mg/dl and in whom total urine output exceeded 1 liter over a four- to six-hour interval ("diuretic" group), no significant change in plasma or total blood volume was observed, nor were there any significant changes in hematocrit. In a "nondiuretic" group of 11 patients who had moderately decreased renal function (blood urea nitrogen level 59.3 +/- 13.0 mg/dl and serum creatinine level 2.3 +/- 0.3 mg/dl) and in whom total urine output was less than 1 liter over the four- to six-hour interval, there was a significant increase in blood volume with a concomitant decrease in hematocrit and hemoglobin levels. Furosemide-induced diuresis therefore did not deplete intravascular volume. To the contrary, actions of furosemide that were independent of its diuretic action were associated with an expansion of plasma volume in the absence of diuresis. This may be related to the venous capacitance effects of furosemide with lowering of venous resistance and, therefore, lowering of the capillary hydrostatic pressure. In addition, there was an increase in colloid osmotic pressure. Both mechanisms increase the effective oncotic pressure gradient, which favors reabsorption of extravascular (edema) fluid. It is concluded that intravascular volume was therefore replenished at a rate equal to or in excess of the volume removed by diuresis.
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PMID:Blood volume following diuresis induced by furosemide. 671 72

Air pollution may affect athletic performance. In Los Angeles, contaminants include carbon monoxide, ozone, peroxyacetylnitrate (PAN) and nitrogen oxides, whereas in older European cities, such as Sarajevo, "reducing smog" of sulfur dioxide is the main hazard. The carbon monoxide and ozone levels expected in Los Angeles this summer could affect the athletes' performance in endurance events at the Olympic Games. Carbon monoxide may also impair psychomotor abilities, and PAN causes visual disturbances. The only likely physiologic consequence from reducing smog is an increase in the workload of the respiratory system and thus a decrease in endurance performance. While carbon monoxide has been blamed for myocardial infarctions, nitrogen oxides for pulmonary edema and sulfur dioxide for deaths due to respiratory failure, the only illnesses that are likely to be more frequent than usual among young athletes exposed to high levels of these pollutants are upper respiratory tract infections. Therapeutic tactics include the avoidance of pollution, the administration of oxygen, vitamin C and vitamin E, and general reassurance.
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PMID:Athletic performance and urban air pollution. 674 56

The LC50 of nitrogen trichloride (NCl3) was determined in rats following a one hour inhalation exposure. Five groups of 10 animals per group were exposed to a concentration range of NCl3 from 58 ppm to 157 ppm. The one hour LC50 is 112 ppm with the 95% confidence interval between 107 ppm and 117 ppm. All mortality occurred during or within one day following the exposure. Gross necropsy of the animals which died as a result of exposure to NCl3 showed noticeable fluid in the trachea and lungs. This was not the case for those animals which survived the exposure (gross necropsies performed 14 days post-exposure). Pulmonary edema appears to contribute significantly to mortality produced by NCl3.
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PMID:Acute inhalation toxicology of nitrogen trichloride. 683 41

Acute edematous lung injury is associated with a marked increase in the number of granulocytes in the alveoli and microvasculature of the lung. Phorbol myristate acetate (PMA) causes granulocytes to adhere, aggregate, and release oxygen radicals and granular enzymes. We found that intravenously injected PMA caused a protein-rich edema in lungs of control rabbits but not in granulocytopenic rabbits pretreated with nitrogen mustard. Specifically, control rabbits treated with PMA had higher lung weight to body weight ratios (6.4 +/- 1.0 X 10(-3)) and lung lavage albumin concentrations (190 +/- 44 mg/dl) than granulocytopenic rabbits pretreated with nitrogen mustard and then given PMA (4.74 +/- 0.23 X 10(-3) and 9.9 +/- 3.8 mg/dl, respectively). To further clarify the role of granulocytes in the production of edema, additional experiments were conducted in an isolated perfused rabbit lung. Addition of purified granulocytes and PMA to the balanced salt perfusate caused lung edema, whereas neither granulocytes nor PMA alone caused edema. Specifically, increases in lung weights (42 +/- 9.2 g) and albumin concentrations (1,182 +/- mg/dl) in lung lavages from isolated lungs exposed to granulocytes and PMA were greater than increases in lung weights or albumin concentrations in lung lavages from isolated lungs exposed to granulocytes alone (2.0 +/- 0.4 g and 15 +/- 0.6 mg/dl), or to PMA alone (6.0 +/- 0.6 g and 81 +/- 34 mg/dl). To determine the contribution of oxygen radicals to the pathogenesis of the edema, chronic granulomatous disease granulocytes, which are deficient in oxygen radical production, were added to the isolated lung perfusate. Chronic granulomatous disease granulocytes and PMA did not cause edema in isolated lungs (delta lung weight 1.0 +/- 0.2 g and lavage albumin 12 +/- 5.0 mg/dl) whereas granulocytes from normal human subjects and PMA did (delta lung weight 43 +/- 5.2 g and lavage albumin 1,120 +/- 54 mg/dl). These data suggest that oxygen radicals released from stimulated granulocytes contribute to the pathogenesis of acute edematous lung injury.
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PMID:Granulocytes mediate acute edematous lung injury in rabbits and in isolated rabbit lungs perfused with phorbol myristate acetate: role of oxygen radicals. 707 14

Atelectasis, pulmonary edema, fibrosis, pneumothorax, and mucous plug airway obstruction all result in reduced lung volume. The oxygen (O2) wash-in method provides a way to monitor routinely the functional residual capacity (FRC) in the ICU without disconnecting the patient from the ventilator and without additional personnel or instrumentation. This method is a modification of an open-circuit nitrogen (N2) wash-out procedure and requires a computer-based respiratory monitoring system with a fast response O2 analyzer and respiratory flowmeter. FRC is computed after a 20% or greater change in the ventilator FIO2 setting. The accuracy and reproducibility of the method were evaluated using artificial lungs, normal subjects, and postcardiac surgery patients. FRC estimates by O2 wash-in and helium dilution were highly correlated, with r = 0.97 and a regression slope and zero intercept of 1.06 and -0.13, respectively. The FRC difference between 23 repeated trials in 18 postcardiac surgery patients was 70 +/- 160 ml (mean +/- SD).
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PMID:Oxygen wash-in method for monitoring functional residual capacity. 709 1

Pretreatment with cycloheximide or emetine provided significant protection against pulmonary edema in rats exposed to ozone or nitrogen dioxide. Other inhibitors of protein-synthesis, actinomycin D or puromycin, failed to show such effects. Possible actions of these agents as well as the doses and times that afforded the significant protection were investigated. These agents, by themselves, did not alter the water content of the lungs. In vitro study revealed that both cycloheximide and emetine hardly acted as scavengers of oxidant. Pretreatment with either agent was associated with a significant increase in the activity of glucose 6-phosphate dehydrogenase of the lungs, but the increase did not necessarily coincide with the protection. Activity levels of non-protein SH, glutathione-peroxidase and -reductase in the lungs of rats treated with either agent were scarcely altered. The effect of these agents administered in vivo or in vitro on the in vitro lipid peroxidation by air was also investigated. Other possible mechanisms of these agents responsible for the protective effect against pulmonary edema induced by oxidants were also discussed.
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PMID:Protection with cycloheximide or emetine against pulmonary edema induced by ozone or nitrogen dioxide. 713 93

We studied the effects of systemic venous hypertension (SVH) of 25 cmH2O, with and without fluid overload (100 ml.kg-1.h-1 x 4 h), on the lung water content and pulmonary function of anesthetized dogs. SVH was produced by inflating a balloon in the right atrium. Pulmonary extravascular water (PEW) was measured by gravimetric techniques taking the water content of trapped blood into consideration. Subdivisions of lung volume, pulmonary resistance, dynamic compliance, and the single-breath nitrogen washout curve were performed in a body plethysmograph. Vascular pressures, serum oncotic pressure, and arterial blood gases were also measured. Systemic venous hypertension alone produced no change in lung water content (control PEW = 3.46 +/- 0.16; SVH PEW = 3.44 +/- 0.18 g H2O/g dry tissue, mean +/- SD) or alterations in pulmonary function. Fluid overload alone produced an insignificant increase in PEW (4.24 +/- 0.72 g H2O/g dry tissue) and decreases in vital capacity and functional residual capacity. SVH in combination with fluid overload resulted in a significant increase in lung water (4.78 +/- 1.03 g H2O/g dry tissue) and decreases in functional residual capacity, vital capacity, dynamic compliance, and arterial blood oxygen tension as well as increased pulmonary resistance. We conclude that SVH favors the formation of pulmonary edema under conditions of increased pulmonary transcapillary fluid exchange and may particularly augment airway edema.
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PMID:Effect of systemic venous hypertension on pulmonary function and lung water. 732 59

A 17-year-old previously well ice hockey player experienced acute shortness of breath and cough productive of clear frothy sputum about 1.5 hours following an ice hockey match. Noncardiogenic pulmonary edema was found to develop as a result of the inhalation of the oxides of nitrogen. The latter was produced by a Zamboni machine that is used to resurface the ice on a rink. Several other players were affected but less severely.
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PMID:'Zamboni disease'. Pulmonary edema in an ice hockey player. 750 8


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