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

Distinct barrier lesions and an apical-basal distribution of alveolar edema fluid in either moderate or high elevated pressure edema lungs have been found in previous studies. In the present study, quantitative measurements were obtained by using electron microscopy and morphometry of extravascular lung water and barrier lesions, on the relations between interstitial and alveolar edema fluid as well as between extravascular lung water and barrier lesions. The study further addressed the question of whether 6% bovine serum albumin (BSA) perfusion could induce lung ultrastructure alterations. It was found that interstitial fluid distribution is similar to that of alveolar edema fluid. Epithelial blebs are also distributed with an apical-basal gradient, and are always submerged in alveolar edema fluid. Perfusion with 6% bovine serum albumin does not induce any lung ultrastructure alterations. The results indicate that endothelium and epithelium play a different role in controlling fluid movement between capillary and extravascular spaces and thus in preventing the formation of interstitial and alveolar edema. Because the interaction of cells and tissue must be taken into account, simple physiological models of pulmonary fluid exchange may not be adequate to explain pulmonary edema formation.
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PMID:Lung lesions in experimental hydrostatic pulmonary edema: an electron microscopic and morphometric study. 855 90

We studied methods for diagnosing the acute respiratory distress syndrome (ARDS) based on its characteristic abnormalities. A gamma-ray external counting method with Tc-99m human serum albumin revealed that pulmonary microvascular permeability was abnormally high in patients with ARDS. With this method, ARDS could be distinguished from cardiogenic pulmonary edema. Levels of interleukin-8 in bronchoalveolar fluid from patients with septic ARDS, reexpansion pulmonary edema, and inhalation burn injury were abnormally high. In 21 patients with acute lung injury, 15 of whom had ARDS, plasma concentrations of three inflammatory markers were measured: thiobarbituric acid reactive material which reflects cell membrane lipid peroxidation; 7S collagen, a component of basement membrane; and the soluble form of P-selectin, an adhesion molecule. Levels of all three were abnormally high in patients with ARDS, and correlated with the degree of lung injury and with the outcome in these patients. We conclude that these measurements in plasma or bronchoalveolar lavage fluid may enable us to assess the severity of ARDS.
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PMID:[Pathophysiology and Diagnosis of the acute respiratory distress syndrome]. 875 14

Isolated lungs from male Wistar rats (250-350 g) were perfused at a constant flow rate (10 ml/min, non-recirculating) with Krebs-Ringer-bicarbonate buffer containing 4.5 % bovine serum albumin, and were ventilated at a positive pressure (60 breaths/min). Pulmonary arterial pressure and lung weight (as a measure of edema formation) were recorded continuously. After an equilibration period of 20 minutes the various test compounds were added to the perfusion fluid and experimental recording was continued for another 60 minutes. The effects of the stable PGI2-mimetic, iloprost, of PGE1, and of the biologically active PGE1-metabolite, 13,14-dihydro-PGE1, were evaluated in this model (n = 6). Iloprost showed slight, but not significant vasodilation; however, lung weight remained unchanged. PGE1 and 13, 14-dihydro-PGE1 also caused slight vasodilation, but in contrast to iloprost these compounds induced distinct pulmonary edema. The lung weight gain was discernible at concentrations of 2.8 x 10(-6) mol/l (significant at 2.8 x 10(-5) mol/l; p < or = 0.05) and was accompanied by increases in the wet-weight to dry-weight ratios. These findings were duplicated in a second set of experiments (n = 6) from which the same results were obtained. The results indicate that at high concentrations PGE1 (and 13,14-dihydro-PGE1), but not iloprost, can induce pulmonary edema in rats probably by increasing the permeability of the pulmonary vasculature.
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PMID:A comparative study of the effects of iloprost and PGE1 on pulmonary arterial pressure and edema formation in the isolated perfused rat lung model. 884 48

It is well known that verocytotoxin-producing Escherichia coli O-157 : H7 infection can be severe in elderly persons. We report an 82-year-old female case of verocytotoxin-producing Escherichia coli O-157 : H7 infection. She was admitted to our hospital because of bloody diarrhea. The hemolytic-uremic syndrome (HUS) was not occurred, but systemic edema, ascites, pleural effusion and pulmonary edema with hypoxyemia gradually appeared. Treatment with human immunoglobulin in addition to fluid therapy, antibiotics, diuretics and human serum albumin resulted in dramatic improvement. Management of complications such as sepsis and electrolyte disturbance caused by this infection was considered to be important in elderly patients.
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PMID:[An old female case of vero-cytotoxin-producing Escherichia coli O-157: H7 infection]. 915 16

Increased microvascular permeability and mucosal edema are pathological features of airway inflammation in asthma. In this study, we investigated the characteristics of the edema response occurring in a model of antigen-induced lung inflammation in sensitized brown Norway rats and examined the effects of monoclonal antibodies (mAbs) to adhesion molecules on this response. Ovalbumin (OA) challenge-induced increases in lung permeability were determined by the leakage of 125I-labeled bovine serum albumin (BSA) into the extravascular tissues of the lungs 24 h after challenge in animals intravenously injected (prechallenge) with this tracer. Inflammatory cell infiltration into the alveolar space was determined by bronchoalveolar lavage (BAL). Mean extravascular plasma volume in the lung increased 233% as compared with control (P < 0.005) at 24 h and increased to 517% by 72 h. The 24-h edema response was completely inhibited by two oral doses (0.1 mg/kg) of dexamethasone 1 h before, and 7 h after, challenge. Intraperitoneal administration of the anti-rat ICAM-1 mAb 1A29, or anti-rat alpha4 integrin mAb TA-2 (2 mg/kg at 12 and 1 h before, and 7 h after, antigen challenge), significantly suppressed eosinophil infiltration into the alveolar space without inhibiting the enhanced microvascular leakage and lung edema. Determination of plasma antibody concentrations by ELISA of mouse IgG1 indicated that sufficient concentrations of the appropriate mAb were present to block alpha4- or ICAM-1-dependent adhesion. The results suggest that increases in microvascular permeability and plasma leakage occurred independently of eosinophil accumulation.
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PMID:Roles of adhesion molecules ICAM-1 and alpha4 integrin in antigen-induced changes in microvascular permeability associated with lung inflammation in sensitized brown Norway rats. 940 63

The postoperative courses of 112 patients with pulmonary disease (59 with obstructive disease = Group 0, 38 with restrictive disease = Group R and 15 with mixed disease = Group M) who underwent elective coronary artery bypass grafting were retrospectively reviewed. Preoperative pulmonary function test (percentage of vital capacity = %VC and percentage of forced expiratory volume at 1 second = FEV1.0%) of these group showed typical abnormal values, and velocity ratio of 50% and 25% of maximum expiratory flow volume (V50/V25) of each groups were measured abnormal values (3.99 +/- 1.44 of Group O, 4.26 +/- 1.42 of Group R and 3.74 +/- 1.82 of Group M). The our strategy for these groups were a). Using skeletonization method for harvesting internal mammary artery (IMA) b) Take care not to injure the phrenic nerve and open the pleural cavity as surgical techniques (Harvesting IMA) and c) Administration of theophylline derivatives and corticosteroids to prevent bronchospasm d) Administration of concentrated serum albumin and diuretics to prevent pulmonary edema as therapeutic measures. The length of stay in the intensive care unit and ventilation time of each groups were not significantly longer. Patients of group M had more respiratory complications (atelectasis, pleural effusion, pneumothrax, bronchospasm, and pneumonia) than did patients of group R (p < 0.05), but did not more nonpulmonary complications and hospital deaths. The four in hospital deaths (2 with group O, 1 with group R and 1 with group M) were not directly related to pulmonary complications. Thus, result of CABG in patients with pulmonary impairment definitely proved to be satisfactory by our strategy, but mixed pulmonary diseased significantly had more pulmonary complications.
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PMID:[Postoperative complications after coronary bypass operations in patients with pulmonary impairment]. 955 57

It is well known that scorpion venom induces lung lesions and respiratory distress which are usually classified as pulmonary oedema (PO). Tityus discrepans is a scorpion that lives in the north-central area of Venezuela, is the most common source of human envenomation here and produces PO. We studied the action of the venom of Tityus discrepans on whole rabbits and on their isolated lungs perfused with Krebs saline with 1 g/l of bovine serum albumin (Krebs-BSA saline). Two milligram of venom were diluted in 250 ml of solution (approximately the rabbit's total blood volume) and used to perfuse isolated lungs. Lung oedema occurred in rabbits which received 1 mg/kg of scorpion venom i.p., heparin prevented the production of this lung oedema. T. discrepans venom produced PO, in rabbits pretreated with 15 mg/kg of ajoene. Yet, Tityus venom had no effects on isolated lungs perfused with citrated or heparinized blood, and in lungs perfused with Krebs-BSA with normal Ca2+. These result show that Tityus venom does not act directly on lungs. Otherwise, we have observed that abundant microthrombi occurred in all rabbit lungs exposed to venom in vivo, suggesting that these clotting alterations are fundamental to produce PO. The presence of intravascular microthrombi is not characteristic of the usual PO hinting that scorpion venom induced pulmonary alterations are a different clinical entity. We thus propose that the use of the term pulmonary oedema in scorpionism should abandoned in favor of scorpion venom respiratory distress syndrome.
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PMID:Tityus discrepans venom produces a respiratory distress syndrome in rabbits through an indirect mechanism. 992 Apr 89

Bolus intravenous injections of phosphorothioate oligonucleotides (PS-ODN) into primates cause profound hypotension, which has been attributed to complement activation, the biochemical pathway leading to acute inflammatory response. Because the hypotension was not accompanied by peripheral or pulmonary edema and epinephrine was not effective, but administration of 200 ml Ringer's lactate was effective, we examined the possibility that the 15-base PS-ODN interferes with sympathetic tone. We administered doses ranging from 3.3 to 10 mg/kg of a 15-base PS-ODN as a 30-60 s iv bolus into the right atrium of conscious Macaca mulatta. Blood pressure fell to 27 mm Hg following a 5.0 mg/kg dose, but no hypotension was observed after a 3.3 mg/kg dose; 10 mg/kg was lethal. Adrenergic receptor binding was evaluated in radioligand binding assays using rat cerebral cortex membranes with radiolabeled prazosin. The 15-base PS-ODN competes with prazosin for the alpha(1)-adrenergic receptor with an IC50 of 14 microM, which favors binding over serum albumin (K(d) = 37 to 48 microM). Admixing serum albumin with 5.0 mg/kg 15-base PS-ODN prior to injection prevented hypotension, suggesting that unbound PS-ODN interferes with sympathetic tone before binding to plasma proteins. Interactions of the 15-base PS-ODN with the alpha(1)-adrenergic receptor in vivo were confirmed by a decreased response to phenylephrine. Reducing the length from 15 to 9 or 5 bases abolished alpha(1)-adrenergic receptor binding in vitro and bolus infusion of 5.0 mg/kg of 9-base PS-ODN no longer produced hypotension. In conclusion, the 15-base PS-ODN shows cooperative binding to the alpha(1)-adrenergic receptor, which produces cardiovascular effects that are oligomer length, dose, and formulation dependent.
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PMID:Bolus intravenous injection of phosphorothioate oligonucleotides causes hypotension by acting as alpha(1)-adrenergic receptor antagonists. 1054 63

1. Unlike in normal rabbits, pulmonary rapidly adapting receptors (RARs) in rabbits with chronic mitral regurgitation (MR) do not respond to small changes in extravascular fluid (EVF) volume in major airways. The present study examined the effect of shrinking the EVF volume in rabbits with chronic MR by infusing hypertonic albumin, to see whether this response of RARs is restored. The effect of raising the left atrial pressure (LAP) acutely above 25 mmHg (to cause pulmonary oedema) on RARs was also investigated. 2. Mean RAR activities in rabbits with MR (n = 6) at initial control, LAP +5 mmHg, LAP +10 mmHg and final control periods were 20.9 +/- 9. 5, 18.8 +/- 11.3, 27.0 +/- 11.2 and 17.2 +/- 9.8 action potentials min-1, respectively (P > 0.05, ANOVA). After infusion of 35 % bovine serum albumin i.v. these values were 9.4 +/- 3.2, 30.6 +/- 14.6, 48. 9 +/- 10.1 and 18.4 +/- 7.3 action potentials min-1, respectively (P < 0.01, ANOVA). In rabbits with chronic MR (n = 7) raising the LAP above 25 mmHg stimulated RARs. 3. EVF content of the airways and lungs was measured in rabbits with MR and in control rabbits, at baseline and after elevation of the LAP by 10 or 25 mmHg for 20 min. In control rabbits the EVF contents in the lower trachea, carina and bronchi at baseline and at LAP +10 mmHg were 52.1 +/- 1.2 and 57.8 +/- 1.7 %, respectively (P < 0.05, Student's t test). In rabbits with MR these values were 58.3 +/- 1.5 and 56.9 +/- 1.9 %, respectively. When the LAP was elevated by 25 mmHg the EVF content increased to 62.4 +/- 1.1 % (P < 0.05, t test compared with baseline and LAP +10 mmHg). 4. We concluded that in rabbits with chronic MR, RARs are unable to respond to acute, small elevations of LAP because there is no concomitant increase in EVF content in the vicinity of these receptors. Furthermore, these receptors can be activated in these animals by elevating the LAP above 25 mmHg or can be made sensitive to acute small elevations of LAP by shrinking the chronically expanded EVF compartment.
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PMID:Rapidly adapting receptors in a rabbit model of mitral regurgitation. 1060 3

Endogenous lung surfactant, and lung surfactant replacements used to treat respiratory distress syndrome, can be inactivated during lung edema, most likely by serum proteins. Serum albumin shows a concentration-dependent surface pressure that can exceed the respreading pressure of collapsed monolayers in vitro. Under these conditions, the collapsed surfactant monolayer can not respread to cover the interface, leading to higher minimum surface tensions and alterations in isotherms and morphology. This is an unusual example of a blocked phase transition (collapsed to monolayer form) inhibiting bioactivity. The concentration-dependent surface activity of other common surfactant inhibitors including fibrinogen and lysolipids correlates well with their effectiveness as inhibitors. These results show that respreading pressure may be as important as the minimum surface tension in the design of replacement surfactants for respiratory distress syndrome.
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PMID:A concentration-dependent mechanism by which serum albumin inactivates replacement lung surfactants. 1180 25


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