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

The object of this study was to determine how pulmonary edema affects the volume of gas trapped in excised lungs as they are slowly ventilated. In this study trapped gas is defined as the volume of gas that cannot be removed from the lungs with a negative transpulmonary pressure of -5 cm H2O (Frazer and Weber, 1976). Experimental pulmonary edema was produced by ventilating rats using high inspiratory positive pressure breathing (HIPPB) as described by Webb and Tierney (1974). The amount of gas trapped in both edematous and control lungs was then compared as the lungs were inflated-deflated under identical conditions in 6 different 4 cycle sequences. During each sequence the lungs were deflated to an end expiratory pressure of either +6, +4, +3, +2, 0.0, or -5 cm H2O. It was found, that gas became trapped at more positive values of end expiratory pressure in lungs having pulmonary edema than in control lungs. These results were interpreted as evidence that the airways close sooner, at more positive transpulmonary pressures, in edematous lungs than in control lungs.
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PMID:The effect of pulmonary edema on gas trapping in excised rat lungs. 52 48

The effect of unilateral pulmonary microembolization on regional lung extravascular fluid accumulation was determined in dogs. Embolization was produced by injecting 100-micrometer-diam glass beads (0.25 g/kg) into the right pulmonary artery. After embolization of one lung, pulmonary arterial pressure (Ppa) and pulmonary vascular resistance increased (P less than 0.05) from base-line values of 11.7 +/- 1.3 to 17.9 +/- 1.3 Torr and of 3.4 +/- 0.5 to 5.5 +/- 0.5 Torr/(1/min). Blood flow to embolized lung measured with labeled microspheres decreased from 104.2 +/- 24.9 to 35.2 +/- 9.2 ml/min.g bloodless lung after embolization, whereas flow to the normal lung increased from 43.1 +/- 5.6 to 71.2 +/- 19.2 ml/min.g bloodless lung. Extravascular lung water-to-bloodless dry lung weight ratio (W/D) of 4.97 +/- 0.32 was greater (P less than 0.001) in the embolized lung than the value of 3.34 +/- 0.15 in nonembolized lung. In six dogs pretreated with 500 U/kg of heparin, a similar degree of duration of embolization and similar hemodynamic changes did not result in significant differences in W/D (3.88 +/- 0.18 in right lung vs. 3.02 +/- 0.53 in the left lung), and the right lung ratio was less (P less than 0.05) than the value in the heparinized dogs, suggesting that humoral mechanisms contribute to the genesis of pulmonary edema after regional embolization. Therefore, unilateral embolization leads to a greater increase in extravascular content in the embolized lung than in the nonembolized lung. Because Ppa was in the normal range after embolization, regional pulmonary edema may be due partly to the local release of factors that increase lung vascular permeability.
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PMID:Site of pulmonary edema after unilateral microembolization. 53 50

We evaluated the attenuation of the 122 keV gamma ray of cobalt-57 across the thorax of anesthetized dogs as a method for following the time course of lung water changes in acute pulmonary edema induced by either increased microvascular permeability or increased microvascular hydrostatic pressure. The gamma rays traversed the thorax centered on the seventh rib laterally where the lung mass in the beam path was greatest. Calibration measurements in isolated lung lobes demonstrated the high sensitivity and inherent accuracy of the method over a wide range of lung water contents. In control dogs reproducibility averaged +/-3%. Increased permeability edema led to large rapid increases in the transthoracic gamma ray attenuation (TGA), while increased pressure caused an immediate, modest increase in TGA (vascular congestion) followed by a slow further increase over 2 h. There was a fairly good correlation between the increase in extravascular lung water and the change in TGA. The method is simple, safe, and noninvasive and appears to be useful for following the time course of lung water accumulation in generalized lung edema in anesthetized animals.
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PMID:Measurement of pulmonary edema in intact dogs by transthoracic gamma-ray attenuation. 53 94

We measured the flux of albumin between the vascular space and the pulmonary interstitial and luminal lining fluids in 20 adult sheep with chronic lung lymph fistulas. We sampled the bronchoalveolar lining layer by episodic fiberbronchoscopic lavage. A total of 62 alveolar lavages were performed at times ranging between 30 min and 60 h after intra-arterial injection of 100 microCi of 125I-labeled albumin. Samples of lymph and plasma were obtained simultaneously with lavage fluid, and the radioactivity and albumin content of all samples were measured and expressed as specific activity (counts/min . g albumin). We found that alveolar lavage fluid collected by our technique is not significantly contaminated by plasma or interstitial fluid proteins. Proteins present in alveolar lavage fluid and also present in plasma reach the alveolar space by a normal diffusive process, and not as a result of epithelial membrane damage occurring at the time of lavage. Lung epithelial permeability to albumin in small, but finite (4.3--5.8 x 10(-10) cm/s). Virtually all (greater than 92%) of resistance to albumin flux across the alveolocapillary membrane lies in the epithelial barrier. Increases in permeability of the respiratory epithelium, even minor, would have a marked effect on water and solute balance in the lung. Epithelial injury will potentiate pulmonary edema formation even in the presence of normal pulmonary microvascular pressure, plasma oncotic pressure, and endothelial permeability.
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PMID:Differential permeability of endothelial and epithelial barriers to albumin flux. 53 3

The effects of hemorrhage on pulmonary hemodynamics and lung transvascular fluid dynamics were studied in sheep. We found that 2 hr of hemorrhage caused a fall in lung lymph flow (p less than 0.05) and no significant change in lymph protein concentration. The fall in lymph flow was not due to decreased vascular surface area since the regional distribution of pulmonary perfusion was not altered during hemorrhage; however, the decrease in lymph flow was associated with decrease (p less than 0.05) in the calculated pulmonary microvascular pressure. The extravascular lung water lung content per g bloodless dry lung was increased (p less than 0.05) in the hemorrhaged sheep from the control values. Pulmonary edema was not due to increased lung vascular endothelial permeability since the net transvascular protein flux was not increased. The finding that pulmonary edema occurred despite the consistent decreases in lymph flow suggests that edema may be due to hemorrhage-induced lymphatic "failure" or that edema fluid is sequestered in spaces (e.g., endothelial cells) where if cannot be drained by the lymphatics.
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PMID:Pulmonary transvascular fluid dynamics in sheep during hemorrhage. 54 20

Intravenous administration of porcine pancreatic elastase to hamsters produced significant loss of elastic recoil at low volumes. Histology and mean linear intercept of the lungs fixed at a pressure of 20 cm H2O and studied for 3 weeks after administration of elastase were normal. Larger doses of elastase caused immediate fatal, hemorrhagic pulmonary edema. These results confirmed previous morphologic observations of the effects of intravenously administered elastase, but demonstrated that the loss of elastic recoil at low lung volumes is not invariably associated with histologic changes or morphologically with loss of elastin fibers. These observations suggest that submicroscopic lesions may be present and may antedate the earliest morphologic evidence of emphysema and aging in the lung.
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PMID:Physiologic and morphologic observations of the effects of intravenous elastase on the lung. 61 30

Intravenous administration of ethchlorvynol (Placidyl) is known to produce noncardiogenic pulmonary edema in animals and humans. Since intrapulmonary sequestration of leukocytes has been observed to occur following injection of ethchlorvynol, we evaluated the role of these elements of the blood in producing pulmonary edema. In vivo studies in dogs showed intrapulmonary trapping of leukocytes, as evidenced by increasing leukocyte differences between blood from the pulmonary artery and arterial blood. In both animals with normal leukocyte counts and those depleted of leukocytes (less than 500 cells per millimeter), pulmonary edema occurred, as evidenced by increased pulmonary water after injection of ethchlorvynol. Preparations of isolated lung perfused with either whole blood or leukocyte-poor plasma had similar gains in weight following injection of ethchlorvynol, in spite of marked differences in leukocyte counts. We conclude that intrapulmonary sequestered leukocytes do not play a role in ethchlorvynol-induced pulmonary edema.
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PMID:The role of leukocytes in ethchlorvynol-induced pulmonary edema. 62 May 61

Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p less than 0.05) and lung blood (p less than 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected. This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.
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PMID:Experimental neurogenic pulmonary edema in cats. 63 62

The ability of the portable chest x-ray film to define the amount of physiologic shunting and the severity of noncardiogenic pulmonary edema was evaluated in thirty-seven observations of eleven patients. Ten of the eleven patients were suffering from acute respiratory failure. The radiologic assessment of the amount of pulmonary edema and the severity of left ventricular failure were compared with the physiologic shunt fraction, tracer-measured lung water, and pulmonary arterial wedge pressure. The radiologic scores for edema did not predict the shunt fraction or tracer measurements of lung water. The radiologic score for congestive failure correlated with the wedge pressure but not well enough to be clinically useful. Five per cent of the x-ray results were false-positive and 11 per cent false-negative. Results indicate that the portable chest x-ray technic does not provide quantitative information regarding cardiopulmonary function. It is especially hazardous to accept an x-ray diagnosis of congestive failure as the cause of pulmonary edema.
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PMID:Diagnostic value of the portable chest x-ray technic in pulmonary edema. 63 9

Pulmonary extravascular water has been measured as lung thermal volume (LTV) in a group of nine burned patients. Transducer-detectable indicators were used to permit frequent repetition and quick results. Concurrent recordings were made of cardiac output, pulmonary capillary wedge pressure and the usual hemodynamic variables. Moderate elevation of LTV was seen in all, reaching a maximum value before peripheral edema formation was complete. Left heart filling pressures were low as plasma albumin concentration. Clinical pulmonary edema occurred in one patient treated mostly with crystalloid solution. In several, a secondary peak coincided with edema mobilization.
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PMID:Lung water changes after thermal burns. An observational study. 63 85


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