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

Albumin is the most effective oncotic agent and has wide clinical application. In the resuscitation of injured patients with hypovolemic shock (during war and peace) the use of supplemental albumin is purported to be more effective in restoring plasma volume, increasing cardiac output, preventing pulmonary oedema and maintaining organ perfusion than resuscitation without supplemental albumin. Most important in a study of albumin are criterias for appropriate use because it was sometimes unjustified. Therapeutic use of albumin should not be dictated by arbitrary or pragmatic restriction but rather by rational prescribing from physicians well educated in its use.
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PMID:[Albumin and its therapeutic use - Part II]. 26 69

Fluid conductance and protein permeability have been studied in isolated perfused lung models of pulmonary edema. However, previous studies have not investigated changes of both fluid conductance and protein permeability in the same isolated lung preparation after injury. Arachidonic acid (AA) metabolites are involved in the inflammatory processes that lead to the development of pulmonary edema. The hemodynamic effects of AA have been well established; however, controversy exists concerning the ability of AA to alter the permeability of the pulmonary microvasculature to fluid and protein. The purpose of this study was to simultaneously determine whether transvascular fluid conductance and protein permeability are increased in isolated perfused rabbit lungs with pulmonary edema induced by AA. Indomethacin (80 microM) was added to the perfusate to inhibit the hemodynamic effects of AA and produce a pressure-independent model of pulmonary edema. Fluid conductance was assessed by determination of the capillary filtration coefficient (Kf), and protein permeability was evaluated by measurement of 125I-albumin clearance. The injection of AA (3 mg/200 ml of perfusate) into the pulmonary arterial catheter resulted in an increase in lung weight over the remaining 30-min experimental period. Kf (microliter.s-1 x cmH2O-1 x g dry lung-1) was increased (P < 0.05) in AA-treated lungs at 10 and 30 min post-AA injection when compared with control lungs and baseline values (determined 10 min before AA injection). Albumin clearance was also greater (P < 0.05) in lungs that received AA. 125I-albumin clearance was measured at different rates of fluid flux produced by elevation of venous pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Simultaneous measurement of fluid and protein permeability in isolated rabbit lungs during edema. 149 Sep 56

We have determined regional lung interstitial fluid albumin concentration in lambs with hydrostatic pulmonary edema and correlated it with lung lymph and plasma albumin concentrations. In anesthetized lambs, we raised left atrial pressure to 25-30 cmH2O by obstructing the aorta and volume overloading the lambs with infusions of Ringer lactate solution (group I, n = 10) or sheep's blood (group II, n = 9). We measured lung lymph flow and concentrations of total protein and albumin in plasma and lymph. With micropipettes we also collected interstitial fluid from interlobular septal pools and peribronchial, periarterial, and perivenous liquid cuffs near the hilum for measurement of albumin concentration by the gel immunoelectrophoresis method. In both groups, lung lymph flow increased with left atrial hypertension, and the ratio of lymph to plasma protein concentration fell. For group I, plasma and lymph albumin concentrations during the phase of hydrostatic edema were 1.97 +/- 0.49 and 1.15 +/- 0.36, respectively; for group II, they were 3.77 +/- 0.42 and 2.43 +/- 0.39 g/dl, respectively. Lung wet-to-dry weight ratio averaged 6.0 in both groups. Albumin concentration was always lower in interstitial fluid than in plasma. In both groups, albumin concentration was similar in periarterial and peribronchial fluid cuffs (group I 1.19 +/- 0.6 and 1.36 +/- 0.79 g/dl, respectively; group II 2.87 +/- 1.05 and 2.33 +/- 0.58 g/dl, respectively) but was always greater than that in perivenous and interlobular septal pools (group I 0.61 +/- 0.21 and 0.67 +/- 0.23 g/dl, respectively; group II 1.76 +/- 0.49 and 1.55 +/- 0.52 g/dl, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional differences in interstitial fluid albumin concentration in edematous lamb lungs. 155 50

Lung injury induced by phospholipase A2 (PLA2, 0.046 IU/ml perfusate) was studied in a continuous weighing system of isolated perfused guinea pig lungs. The results revealed that lung weight increased progressively during the 30-min perfusion of PLA2. No change of pulmonary arterial pressure was observed in the same period. Albumin permeability-surface area product, lung index, lung water content, exudate from pleura, and angiotensin-converting-enzyme activity increased significantly at the end of 30 min PLA2 perfusion. p-Bromophenacyl bromide, a PLA2 inhibitor, may block the above changes nearly completely. The effects of inhibitors of cyclooxygenase (indomethacin, IM), lipoxygenase (diethylcarbamaxine, DE), and platelet-activating factor (SRI 63-441) on PLA2-induced lung injury were also studied. We found: (1) PLA2 may induce high permeability lung edema. The role of endothelial injury in the permeability change remains to be further investigated. (2) DE ameliorated lung injury significantly within 10 min of PLA2 treatment but showed no effect after 15 min. IM ameliorated lung injury during the whole experimental period. SRI 63-441 had no effect. It is suggested that PLA2 may damage lung by inducing products of cyclooxygenase and lipoxygenase besides its direct effect.
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PMID:Phospholipase A2-induced lung edema and its mechanism in isolated perfused guinea pig lung. 236 33

In spite of the development of various antibiotics, management of elderly patients with pneumonia remains an important problem. It is suggested that adult respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC) often occur in elderly patients with pneumonia. Although neutrophils are suggested to be involved in the genesis of these conditions, details remain unknown. We demonstrated that a highly cytotoxic substance, 9,10-epoxy-12-octadecenoate, is biosynthesized from linoleate by human neutrophils, thus it was named leukotoxin. Leukotoxin was detected in lung lavages from patients with ARDS. In these lung lavages, increases in albumin concentration and angiotensin converting enzyme (ACE) activity were also observed. Similar results were observed in lung lavages from rats after exposure to hyperoxia for 60 hours in an experimental model of ARDS. Intravenous administration of leukotoxin (100 mumol/kg) caused lung edema. Albumin concentration and ACE activity were increased in lung lavages of rats receiving leukotoxin. In contrast, these changes were not observed in rats administered with linoleate. Furthermore, administration of leukotoxin (100 mumol/kg) caused coagulation abnormality, i.e., increase in fibrin-fibrinogen degradation products, decrease in fibrinogen, and prolongation of activated partial thromboplastin time and prothrombin time. Administration of linoleate did not induce these changes. It is indicated that O2- was produced by respiratory burst enzyme located in neutrophil plasma membrane, and that hydroxyl radicals derived from O2- by Fenton reaction were responsible for leukotoxin synthesis. From our results, leukotoxin, a product of hydroxyl radicals and linoleate, might be responsible for the genesis of ARDS and DIC.
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PMID:[Leukotoxin and pulmonary injury]. 238 90

Amiodarone (ADR), a new antiarrhythmic drug for life-threatening cardiac arrhythmias, causes pneumonitis or lung fibrosis in a sizeable minority of patients. The cause of lung damage is not known. We have shown that infusion of 10 mg amiodarone into the inflow circuit of ventilated and perfused rabbit lungs causes immediate increase in pulmonary artery pressure (mean +/- SEM) (from 13.6 +/- 1.2 to 40.6 +/- 9.5 mm Hg, p less than 0.01) and pulmonary edema with marked increase in the pulmonary generation of thromboxane and leukotrienes C4 and/or D4. Albumin (2 g%) in the perfusate prevents any increase in lung perfusion pressure or edema formation. When lung perfusion pressure increase is blocked with the combined cyclooxygenase and lipoxygenase inhibitor enolicam sodium (CG5391B, 35 microM in perfusate), significant lung edema still occurs after amiodarone, indicating that amiodarone causes increased alveolar-capillary membrane permeability. Addition of catalase (100 U/ml) or superoxide dismutase and catalase (100 U/ml each) to perfusate fails to protect from amiodarone lung injury. Immediate infusion of amiodarone (10 mg) into lungs ventilated with room air (ADR + RA) causes an increase in lung weight gain from baseline (delta W) of 5.7 +/- 1.5 g/min. Compared with ADR + RA, ventilation of lungs with 4% O2 (delta W = 0.7 +/- 0.3 g/min, p less than 0.05), pretreatment of rabbits for 3 days with butylated hydroxyanisole (BHA, 100 mg/kg/day i.p., delta W = 0.05 +/- 0.02 g/min, p less than 0.01), pretreatment of rabbits for 3 days with vitamin E (Vit E, 300 U/day orally, delta W = 0.6 +/- 0.2 g/min, p less than 0.05), or addition of N-acetylcysteine to the lung perfusate (NAC, 5 mM, delta W = 0.1 +/- 0.08 g/min, p less than 0.01) all protect from lung edema formation after amiodarone. Amiodarone (100 mg) also caused a marked increase in luminol-enhanced lung chemiluminescence, lung production of superoxide anion (O2-), and tissue levels of lung glutathione disulfide. These results suggest that amiodarone causes lung injury by an oxidant mechanism.
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PMID:Amiodarone causes acute oxidant lung injury in ventilated and perfused rabbit lungs. 245 31

We determined the oncotic and cardiovascular effects of a standardised infusion of human albumin (1.2 g/kg over 2 h as a 20% solution) in 12 premature infants on 18 occasions when hypovolaemia was suspected on clinical grounds. Blood volume increased by a median value of 15.5%, and fell to preinfusion values by 3 h post infusion in all but four cases. Albumin concentration and colloid osmotic pressure rose during infusion and remained raised even when blood volume had fallen to preinfusion levels. Blood pressure rose in 3 cases only and heart rate fell by greater than 5 beats/min in 6 cases. Indices of long- and short-term heart rate variability were unchanged, but blood pressure variability fell in the second hour of infusion (P = 0.03), an effect which was independent of changes in lung inflation. No changes in blood gases or oxygenation occurred during infusion and no evidence of pulmonary oedema was found. There were wide variations in oncotic and cardiovascular responses to the standardised infusion both between and within subjects. When human albumin is infused in this manner some protection against respiration-induced variability in blood pressure can result, but the circulatory response may prove difficult to predict in the individual.
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PMID:The cardiovascular and oncotic effects of albumin infusion in premature infants. 260 55

We have observed that neutrophils biosynthesize linoleate epoxide, 9,10-epoxy-12-octadecenoate, and have named it leukotoxin because of its cytotoxic effect. In this experiment, the effect of leukotoxin on the lung was investigated. Acute effect of leukotoxin: Using Wistar rats, leukotoxin (100 mumol/kg) was injected intravenously for the leukotoxin group, and linoleate (100 mumol/kg) for the linoleate group. Physiological saline was injected as the control. Ten min after injection, rats were divided into 3 groups: (1) lungs were isolated, and lung wet weight, and dry weight were measured; (2) lung lavages were performed, and albumin concentration and activity of angiotensin converting enzyme (ACE) were measured; (3) morphological changes were studied by light and electron microscope. After administration of leukotoxin, lung wet weight/body weight ratios and dry weight/wet weight ratios were increased. Albumin concentration and ACE activity in lung lavages were also increased. Pulmonary edema was also confirmed by light microscopic findings. Alveolar epithelial cell damage and endothelium damage were also observed. Linoleate had no significant effect on these biochemical parameters and morphological findings. Subacute effect of leukotoxin: Twelve hr after administration of leukotoxin (50 mumol/kg) or linoleate (50 mumol/kg), the same studies were performed as in the acute experiments. Immediately after administration of leukotoxin, no significant effect was observed. However, 12 hr later similar changes were observed as in the acute experiments. Linoleate did not show any significant effect 12 hr after injection. These results indicate that leukotoxin biosynthesized by neutrophils might be closely related to the genesis of inflammatory edema.
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PMID:Neutrophil-derived epoxide, 9,10-epoxy-12-octadecenoate, induces pulmonary edema. 314 92

Albumin is a much abused and expensive drug in intensive care units. One of the motivations for its use is the prevention of pulmonary edema by enhancing the colloid osmotic pressure (COP). Fear of pulmonary edema has led to the formation of a magic (arbitrary) albumin value varying from one intensive care unit to another. Many intensive care units start substituting albumin when it is below 25 g/l. The objective of this paper is to look at the rationale of this policy. Our results show that in intensive care patients, with a variety of primary diagnoses, a poor correlation exists between COP and serum albumin concentration (r = 0.56; p less than 0.001). To get an index of the colloid osmotic status of the I. C.-patient measuring albumin concentration is useless and COP should be measured instead. From 19 patients with a COP in the 15.0-20.0 mmHg range (corresponding albumin range: 12.0-25.0 g/l) and from 10 patients with a COP in the 11.6-15.0 mmHg range (corresponding albumin range 10.5-19.2 g/l) none developed pulmonary edema. It is questionable if expensive, scarce albumin is the drug of choice with which to increase COP, for the mean increase (+/- SD) in COP after infusion of 100 grams albumin is 2.2 (+/- 1.5) mmHg (p less than 0.001). Adopting a COP action level of 15 mmHg can lead to considerable savings.
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PMID:Albumin abuse in intensive care medicine. 271 9

In order to study the kinetics and pathways of protein transfer in pleural effusion, rats with pleurisy associated with hyperoxic pulmonary edema were injected either intrapleurally or intravenously with tracers. 125I-Albumin was used to obtain quantitative data. Anti horseradish peroxidase used as a morphological tracer, allowed a precise localization of the pathways used for the transfer. It has been possible to demonstrate that, in this model, the pleural effusion is produced by a plasma exudation accumulated in the lung interstitium, transferred through the visceral pleura and resorbed by the lymphatics of the parietal costal and diaphragmatic pleurae.
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PMID:Protein transfer in hyperoxic induced pleural effusion in the rat. 394 10


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