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)

An arterial catheter-bearing external conductivity electrodes and a thermistor was used for measurement of lung thermal volume (LTV) by the double-indicator method. Ten milliliters of 3% saline at room temperature were injected, dilution curves measured, and LTV calculated as mean transit time difference, less thermistor time constant, times cardiac output (CO). Comparisons were made, in dogs, between LTV, pulmonary extravascular lung water with Evans blue and tritiated water (PEVWtho), and weighed lung water (WLW). Pulmonary edema was induced with dextran and epinephrine. CO was measured by thermodilution in both the pulmonary artery (PA) and aorta (AO) and dye dilution in the AO. CO from dye dilution was compared with thermodilution (aortic detection) to detect irreversible loss of thermal indicator. Comparisons showed good correspondence of dye and thermal curves (Y = 0.91X - 0.16 1/min; r = 0.93). LTV is about 120% of WLW in near normal lungs, 90% of WLW in extreme edema. PEVWtho was 60-70% WLW.
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PMID:Rapid estimation of pulmonary extravascular water with an instream catheter. 110 19

Determination of protein transfer across the endothelial barrier or the entire alveolar capillary membrane is critical for investigation of mechanisms leading to pulmonary edema. The purpose of this study was to evaluate Evans blue dye for determination of protein clearance across cultured bovine pulmonary artery endothelial cell monolayers and as a quantitative marker for albumin leakage to the air spaces in isolated perfused rat lungs. Evans blue dye bound tightly to albumin (EBA) as determined by lack of transfer through dialysis membranes and specific elution with albumin from a molecular exclusion column. EBA was equivalent to 125I-labeled albumin for calculation of albumin clearance rates (Calb) across intact and challenged monolayers [Calb (+ vehicle) = 0.12 microliters/min; Calb (+10 nM alpha-thrombin) = 0.47 microliters/min; Calb (+5 mg/ml trypsin) = 1.29 microliters/min]. Transfer of EBA was linear with time in both the endothelial cell monolayer model and the perfused lung. EBA was a sensitive marker for early edema in the perfused lung (before detectable weight gain) as well as for severe edema in the oxidant-injured lung (marked EBA accumulation in lavage fluid) and was a more specific marker for protein transfer than lavage fluid protein. EBA transfer is a convenient, reproducible, and accurate means to assess alterations in vascular permeability.
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PMID:Evans blue dye as a marker of albumin clearance in cultured endothelial monolayer and isolated lung. 144 23

A disturbed water and electrolyte homeostasis is not generally held to be a primary mechanism in the pathogenesis of acute mountain sickness (AMS) and high altitude pulmonary edema (HAPE), but the association of oliguria and weight gain with AMS and HAPE has led to the hypothesis that water retention may be a facilitative mechanism, possibly caused by an effect of hypoxia to release antidiuretic hormone (ADH). To examine the problem, normal Long-Evans rats (N) and the strain with congenital diabetes insipidus (DI) were exposed to hypobaric hypoxia (0.5 atm) for 4 days, and fluid balance in the whole animals and in their lungs was studied. Both strains reduced water intake and were oliguric on acute exposure, but the N rats gained body weight and increased lung water, while the DI rats increased neither body weight nor lung water. Neither strain increased lung blood at high altitude. The oliguria in the DI rats could not have been due to a release of antidiuretic hormone, and was attributed to the diminished water intake in both strains. The protection against HAPE in the DI rats was probably due to their more severe dehydration that exists already in normoxia, and its further increase in hypoxia, compared with N rats.
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PMID:Water balance and lung fluids in rats at high altitude. 160 61

Anesthetized dogs with thoracotomy were injected with Evans blue dye and were exposed acutely (5 min) to wood smoke inhalation. Thin slices from freeze-dried samples were photographed and assessed for periarterial and perivenous cuff area and for blue coloration with a score of 0 to 5. Bloodless extravascular lung water (EVLW) was also measured. The smoke-exposed animals were compared with controls and with animals exposed to alloxan or to high-pressure-induced pulmonary edema. EVLW at 2 h after smoke (6.46 +/- 0.80) was above control value (4.30 +/- 0.63) but not different from the alloxan (6.13 +/- 0.70) or high-pressure (6.88 +/- 1.30) groups. Despite the similarity in EVLW in the edematous lungs, there were marked differences in the intensity of blue color and size of cuffing around arteries and veins: the smoke, alloxan, and high-pressure groups had blue color scores of 1.0 +/- 0.1, 2.9 +/- 0.3, and 0.3 +/- 0.1, respectively. These scores indicated a large increase in microvascular permeability to proteins in the alloxan group, a moderate increase in the smoke group, and minimal change in the high-pressure group. The perivascular cuff area was largest in the alloxan group and moderate in the smoke and high-pressure groups. The cuff area was higher for arteries than for veins in all groups except the 0.5-h smoke group. We conclude that smoke inhalation causes a moderate increase in permeability and EVLW compared with alloxan. The extravascular lung water accumulates preferentially around the arteries, but the size of the perivascular cuff is not similar for all causes of pulmonary edema.
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PMID:Distribution of extravascular lung water after acute smoke inhalation. 238 21

Uncertainty persists concerning the mechanisms responsible for fluid clearance from the lungs after the air spaces become flooded in severe pulmonary edema. In this study, solute and water fluxes were investigated in an isolated, fluid-filled, perfused rabbit lung preparation. These lungs were perfused with physiologic 1.0 or 5.0 g/dl albumin solutions, and the air spaces were flushed and filled with the same solutions. Samples were obtained at intervals from the perfusate, and at the end of 1 or 2 h, fluid was pumped from the trachea into collection tubes. Concentrations of albumin (labeled with Evans blue) in the air space increased by 2.4 +/- 0.7% (SEM) at 1 h and by 7.0 +/- 0.8% at 2 h. Approximately half of the increase at 2 h could be attributed to dehydration (as judged by increases in perfusate and air-space Na+ concentration). Because previous studies have indicated that the movement of labeled protein between these compartments is very slow in this preparation, it can be concluded that fluid is being reabsorbed from the air spaces. However, reabsorption appears to be slower in rabbits than in rats and it is not stimulated by terbutaline, an effect observed in other species. Under control conditions, potassium concentrations in the air-space fluid fell from 4.01 +/- 0.05 (SEM) mEq/L to 3.37 +/- 0.14 mEq/L at 1 h. Concentrations of K+ in the perfusate rose during this interval from 3.95 +/- 0.05 mEq/L to 4.39 +/- 0.08 mEq/L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reabsorption of solutes and water from fluid-filled rabbit lungs. 244 49

The authors continuously observed the effect of Chuanxiongqin on the microcirculation of hamster cheek pouch by use of the Dual-Window Television Automatic Estimating System. It was seen that the caliber of arterioles, the microcirculatory velocity, and blood flow all decreased after local application of noradrenaline and all increased and returned to normal 1 to 30 min after local administration of Chuanxiongqin. Microcirculatory perfusion, however, could not be improved by normal saline or Iluangqi. The effect of Chuanxiongqin on the pulmonary capillary permeability was also investigated in rats. Pulmonary edema was induced in rats by adrenaline administration. Evans blue was injected intravenously and the amount of Evans blue in broncho-alveolar lavage fluid was estimated. It was found that Evans blue was increased in broncho-alveolar fluid of rats with pulmonary edema, and this increase could be lessened by Chuanxiongqin.
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PMID:Effect of chuanxiongqin (tetrame-thylpyrazine) on microcirculatory perfusion in hamsters and capillary permeability in rats. 263 Nov 22

Concentration-time interactions were investigated in young male and female Sprague-Dawley, Long Evans and Fischer-344 rats exposed to hydrogen sulphide for two, four or six hours. Higher concentrations caused more deaths, with no significant difference for duration of exposure. A significant sex effect was noted with 30% mortality in males and 20% in females, with no significant difference among strains. Changes in weight were significant: increasing with concentration, higher in males than in females, different among strains (Fischer-344 less than Sprague Dawley less than Long Evans), and affected by duration of exposure. Lethal concentration values (LC50 and LC10) were estimated, for the pooled data set (n = 456); the probit equation was Y = -5.74749 + 3.8259X where X is log10 dose of hydrogen sulphide in parts per million. The LC50/LC10 values were 644/298 parts per million (902/417 mg m-3) respectively. Individual probit analyses were also performed for strain, hours of exposure and sex. The LC50 and LC10 values for male, female and strain were not different. Significant differences were observed among LC50/LC10 values for hours of exposure (2 h = 587/549 parts per million, 822/769 mg m-3; 4 h = 501/422 parts per million, 701/591 mg m-3; 6 h = 335/299 parts per million, 469/491 mg m-3). There was no effect of spatial position in the exposure chamber on the distribution of mortality. All rats of all strains dying had severe pulmonary edema.
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PMID:Concentration-time interactions in hydrogen sulphide toxicity in rats. 316 19

We investigated mechanisms related to the development of acute lung edema, as induced by oleic acid in adult mongrel dogs. The intravenous injection of oleic acid (0.04 ml/kg) was considered to induce a permeability edema, as an enhancement of transvascular protein clearance was observed after the injection. The effects of oleic acid injection on systemic blood pressure (SBP), pulmonary arterial pressure (PAP), pulmonary arterial wedge pressure (PAWP), cardiac output (CO) and airway pressure (AWP) were measured. A significant decrease in CO and increase in AWP were evident after the injection, but there were no changes in SBP, PAP and PAWP. Treatment of the animals with prostaglandin I2 (PGI2) did not alter the induction of edema by oleic acid. However, the decrease in CO and increase in AWP were normalized by treatment with PGI2. Blood platelet count was not affected by oleic acid given in a dose of 0.04 ml/kg. To determine the direct effect of oleic acid on the vascular endothelium, the agent was injected through a catheter placed in the pulmonary artery. Electron microscopic examination revealed severe vacuolation on the endothelium of the pulmonary artery after only 1 min of exposure to oleic acid. Increased permeation of Evans blue into the subendothelial tissue was also observed with oleic acid treatment, compared with findings in the controls. These results indicate that the lung edema induced by oleic acid is due to an increased protein clearance, probably through a direct toxic effect on the vascular endothelium rather than an indirect toxic effect of chemical mediators released from the aggregated platelets.
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PMID:Mechanisms involved in acute lung edema induced in dogs by oleic acid. 351 Aug 75

The naturally occurring compound, 4-ipomeanol (IPO, 1-[3-furyl]-4-hydroxy-1-pentanone), selectively damages the nonciliated epithelial (Clara) cells of the terminal bronchioles. Because information is not available concerning functional changes in IPO-treated lungs, an investigation was undertaken to evaluate the in vivo pulmonary ventilatory, mechanical, and gas exchange functions of female Long-Evans rats 24 h after treatment with a single intraperitoneal dose of 1 or 5 mg IPO/kg body wt. A preliminary toxicity study established the 24-h LD50 for intraperitoneally administered IPO at 19 +/- 3 (SD) mg/kg. Significant increases in lung fluid occurred in animals treated with 15 mg IPO/kg, and histological evidence of pulmonary edema was observed in animals treated with 10 mg IPO/kg. Treatment of rats with 5 mg IPO/kg caused a significant decrease in tidal volume and a significant increase in respiratory rate and functional residual capacity-to-total lung capacity ratio (%). In rats treated with 1 mg IPO/kg, pulmonary functions were minimally affected. The functional changes observed in IPO-treated animals can be attributed to swelling and possible dysfunction of Clara cells, with subsequent alveolar interstitial edema and stimulation of juxtapulmonary capillary receptors, or to a direct effect of the toxin on respiratory control mechanisms.
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PMID:Effects of the Clara cell toxin, 4-ipomeanol, on pulmonary function in rats. 683 30

We examined the relationship between airway obstruction and plasma extravasation produced by the intravenous administration of the selective NK1 receptor agonist [Sar9, Met(O2)11]-substance P(SP). Conscious guinea-pigs were injected with Evans' blue dye followed by intravenous [Sar9,Met(O2)11]-SP. Animals were killed 3 min later and airway obstruction, determined via excised lung gas volumes, and plasma extravasation in the trachea, mainstem bronchi and intrapulmonary airways quantitated. Maximal plasma protein extravasation occurred at a dose about 30 times less than that required to elicit airway obstruction. Neither the neutral endopeptidase (NEP) inhibitor, thiorphan, or the angiotensin-converting enzyme (ACE) inhibitor, captopril, altered the extravasation response to [Sar9,Met(O2)11]-SP. However, thiorphan alone or combined with captopril produced a small but significant potentiation of the airway obstructive response. The marked difference between pulmonary gas trapping and Evans' blue extravasation responses suggest that [Sar9,Met(O2)11]-SP-induced airway obstruction is not secondary to increased pulmonary edema.
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PMID:Pulmonary actions of the neurokinin1-specific agonist [Sar9,Met(O2)11]-substance P. 753 2


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