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)

Ten anesthetized dogs, 48 h postintravenous 131I-albumin injection, had a segment of lung airspace isolated by a balloon-tipped catheter lodged in a bronchus. An isotonic saline solution containing trace amounts of Blue Dextran, 125I-albumin, and 57Co-cyanocobalamin was instilled into the lung segment. During control periods, lung saline was absorbed at a rate of 0.133% per minute as measured by indicator dilution of Blue Dextran. Only 57Co-cyanocobalamin crossed the epithelium. Acute hemodynamic pulmonary edema was produced by aortic constriction plus saline overload. In pulmonary edema the fluid volume in the airspace increased at the rate of 0.96% per minute, and there was a significant influx of 131I-albumin into the lung saline from the blood in all animals. However, neither 125I-albumin nor Blue Dextran diffused from the airspace into blood during edema; both were merely diluted by fluid influx. The rate of diffusion of 57Co-cyanocobalamin increased fivefold during edema. A small number of discrete breaks in the lung epithelium allowing bulk flow of interstitial fluid is proposed to account for the one-way movement of albumin in hemodynamic alveolar edema.
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PMID:Solute permeability of the alveolar epithelium in acute hemodynamic pulmonary edema in dogs. 1 23

The permeability of the alveolar epithelium following alloxan challenge was studied in dogs by determining transfer of radiolabeled solutes between alveolus and blood. Two days after injection of 131-Ialbumin into the blood, anesthetized dogs had the air space of part of one lung isolated by a balloon catheter lodged in a bronchus. We infused the atelectatis-isolated area with normal saline containing trace amounts of Blue Dextran, 125Ialbumin, and 57Co-cyanocobalamin; challenged six animals with intravenous alloxan, and six animals with alloxan added to the alveolar saline. During the pulmonary edema, 57Co-cyanocabalamin and 125I-albumin appeared in the blood and 131I-albumin entered the alveolar saline. The animals challenged by alveolar instillation showed a greater permeability change (P less than 0.05). The bidirectional transfer of macromolecules indicates that alloxan produces a change in the permeability of the alveolar epithelium, allowing diffusional exchange of macromolecules. Since alveolar flooding in hemodynamic edema does not show a similar change in the permeability of the epithelial lining, alveolar flooding in alloxan edema is not due solely to an effect on the endothelial membrane, but also to a direct effect on the epithelial membrane.
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PMID:Solute permeability of the alveolar epithelium in alloxan edema in dogs. 63 76

Drug-induced noncardiogenic pulmonary edema occurred in a previously patient receiving dextran 40. Dextran 40 should be considered another etiologic factor of drug-induced noncardiogenic pulmonary edema when this syndrome occurs in the absence of known precipitating causes such as shock, aspiration, and overwhelming pneumonia.
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PMID:Dextran 40: another cause of drug-induced noncardiogenic pulmonary edema. 115 47

This review describes the properties and side effects of Hyskon and the implications for the patient and anaesthetist during hysteroscopy. The amount of Hyskon absorbed is dependent on the injection pressure, the extent of tissue trauma, the seal of the hysteroscope around the cervix, and the duration of infusion. The mechanism of pulmonary oedema after absorbtion of Hyskon is fluid overload, and not injury to pulmonary capillary endothelium. The haematological effects are primarily due to haemodilution. However, case reports suggest that Dextran 70 may cause a syndrome resembling disseminated intravascular coagulation. The allergic response to Hyskon consists of both an anaphylactic and an anaphylactoid component. It is recommended that hysteroscopy with Hyskon be limited to 45 min, and that all possible measures be taken to minimize tissue trauma and bleeding. The volume of Hyskon should be limited to less than 500 ml, since pulmonary oedema and coagulopathy have been described with even lesser amounts. The cumulative volume of Hyskon should be monitored frequently and the patient should be closely monitored for signs of impending pulmonary oedema.
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PMID:Anaesthetic implications of 32% Dextran-70 (Hyskon) during hysteroscopy: hysteroscopy syndrome. 128 May 35

We tested the hypothesis that dextran sulfate and heparin sulfate inhibit platelet-activating factor- (PAF) induced pulmonary edema in the isolated perfused guinea pig lung via a charge-dependent mechanism. Dextran sulfate prevented the changes in pulmonary capillary pressure (Ppc, 7.8 +/- 0.9 vs. 14.0 +/- 0.7 cmH2O), lung weight gain (dW, +0.48 +/- 0.29 vs. +8.41 +/- 2.07 g), and pulmonary edema formation or wet-to-dry weight ratio [(W-D)/D, 6.5 +/- 0.3 vs. 13.2 +/- 2.6] occurring 60 min after PAF infusion (10(-11) M) into an isolated lung. The unsulfated form of dextran had no protective effect [Ppc, dW, and (W-D)/D, 11.9 +/- 1.4 cmH2O, +5.33 +/- 2.18 g, and 11.2 +/- 3.2, respectively]. The unrelated anionic compound, heparin sulfate, also inhibited the PAF response [Ppc, dW, and (W-D)/D, 7.0 +/- 0.5 cmH2O, +0.61 +/- 0.32 g, and 6.1 +/- 0.2, respectively], whereas the partially desulfated form of heparin was not effective in inhibiting PAF-induced edema [Ppc, dW, and (W-D)/D, 15.1 +/- 0.7 cmH2O, +6.07 +/- 1.58 g, and 10.0 +/- 1.2, respectively]. When the metachromatic dye crystal violet was used as an indicator of charge interactions, the sulfated compounds interacted with PAF in vitro. The data indicate that PAF-induced pulmonary edema is inhibited by sulfated polysaccharides, possibly via a charge interaction between negatively charged compounds and PAF.
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PMID:Dextran sulfate and heparin sulfate inhibit platelet-activating factor-induced pulmonary edema. 153 12

Hysteroscopy using 32% Dextran-70 in 10% dextrose (Hyskon) is a common outpatient procedure. We report a case of pulmonary edema and coagulopathy in a 38-year-old, 48 kg female who had hysteroscopy and removal of an endocervical polyp using 700 ml of Hyskon over a 2-hour period. Low percutaneous oxygen saturation (SpO2) and vaginal bleeding developed postoperatively. A vaginal hysterectomy was performed. The coagulation profile showed coagulopathy, which was treated with transfusions of fresh frozen plasma and platelets. The patient developed overt pulmonary edema following the hysterectomy and was treated with positive pressure ventilation. The pathophysiology for the development of pulmonary edema and coagulopathy is discussed. Recommended limits for Hyskon volumes and instillation times are emphasized, as is careful recording of these parameters.
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PMID:Pulmonary edema and coagulopathy following intrauterine instillation of 32% dextran-70 (Hyskon). 171 31

This experimental study was undertaken to clarify the role of pancreatic enzymes and endotoxin in the pathogenesis of pulmonary edema in acute pancreatitis, paying special attention to the effects of two different intravenous infusions: lactated Ringer's solution (LR) and Dextran 40 (D40). After acute pancreatitis was induced in dogs by injecting autologous gallbladder bile into the main pancreatic duct, plasma endotoxin levels increased markedly in both the LR and D40 groups, and PaO2 decreased more significantly in the D40 group. Extravascular lung water (EVLW) increased more significantly in the D40 group than in the LR group, in spite of the fact that colloid-hydrostatic pressure gradient (CHPG) had been maintained more efficiently in the D40 group. Significant correlation between EVLW and plasma endotoxin level was delineated in both groups, but the slope of the regression line in the D40 group was much greater than that of the LR group. Infusion of trypsin and elastase into the pulmonary artery in normal dogs caused moderate elevation of EVLW in the D40 group, but there was no significant alteration in the LR group. The changes of PaO2, EVLW, and CHPG after infusion of endotoxin were similar to those in the animals with experimental acute pancreatitis. In conclusion, endotoxin appears to play an important role in the pathogenesis of pancreatitis-induced pulmonary edema by causing an increase in pulmonary vascular permeability, and under these circumstances the infusion of large amount of colloid solution promotes the development of pulmonary edema.
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PMID:[An experimental study on the pathogenesis of pulmonary edema in acute pancreatitis, with special interest to the effects of colloid infusion and the role of endotoxin]. 172 52

We tested the hypothesis that neutrophil sequestration is required for the development of tumor necrosis factor- (TNF) induced neutrophil- (PMN) dependent pulmonary edema. TNF (3.2 X 10(5) U/kg ip) was injected into guinea pigs 18 h before lung isolation. After isolation, the lung was perfused with a phosphate-buffered Ringer solution. Dextran sulfate (mol wt 500,000) prevented the changes in pulmonary capillary pressure (Ppc; 8.5 +/- 0.8 vs. 12.8 +/- 0.8 cmH2O), lung weight gain (dW; +0.240 +/- 0.135 vs. +1.951 +/- 0.311 g), and pulmonary edema formation or wet-to-dry wt ratio [(W - D)/D; 6.6 +/- 0.2 vs. 8.3 +/- 0.5] at 60 min induced by PMN infusion into a TNF-pretreated lung. The unsulfated form of dextran had no protective effect [Ppc, dW, and (W - D)/D at 60 min: 11.9 +/- 0.9 cmH2O, +1.650 +/- 0.255 g, and 7.3 +/- 0.2, respectively], whereas the use of another anionic compound, heparin, inhibited the TNF + PMN response [Ppc, dW, and (W - D)/D at 60 min: 5.6 +/- 0.4 cmH2O, +0.168 +/- 0.0.052 g, and 6.4 +/- 0.2, respectively]. Isolated lungs showed increased PMN myeloperoxidase (MPO) activity compared with control in TNF-treated lungs at baseline and 60 min after PMN infusion. Dextran sulfate, dextran, and heparin inhibited the increase in MPO activity. The data indicate that inhibition of PMN sequestration alone is not sufficient for the inhibition of PMN-mediated TNF-induced hydrostatic pulmonary edema and that a charge-dependent mechanism mediates the protective effect of dextran sulfate.
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PMID:Dextran sulfate inhibits PMN-dependent hydrostatic pulmonary edema induced by tumor necrosis factor. 185 40

We determined the effect of a body burn on pulmonary function. Full-thickness burns varying in size from 25 to 70% of total body surface (TBS), were produced in sheep. Resuscitation was performed with lactated Ringer's. We noted an increase in lung transvascular fluid flux as measured by lymph flow, Q1, during the resuscitation period, varying from one- to threefold over baseline with the degree of increase directly proportional to the burn size. The increase in QL could be totally explained by the degree of hypoproteinemia which was also proportional to burn size. Transient pulmonary hypertension 20 +/- 4 to 26 +/- 5 mm Hg and a decrease in PaO2 from 90 +/- 5 to 83 +/- 6 torr occurred in the 50 and 70% burns as well as a significant decrease in lung compliance. These alterations were not due to pulmonary edema as there was no increase in measured lung water. Also, the increase in QL could be prevented by using a combination of Dextran and protein for resuscitation but this had no effect on the hypertension or hypoxia. Burn lymph and venous plasma thromboxane levels were increased during this period of lung dysfunction. Ibuprofen 12.5 mg/kg preburn and 12.5 mg/kg every 2 hours postburn decreased the degree of dysfunction suggesting a cause and effect relationship.
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PMID:Early lung dysfunction after major burns: role of edema and vasoactive mediators. 241 27

The purpose of this study was to evaluate the mechanism of development of lung edema and to determine adequate components and amounts of transfusion solution after major hepatic resection in normal and Dimethylnitrosamine (DMNA)-induced cirrhotic dogs. The dogs were administered maintenance dose (1-2 ml/kg/h) or large volumes (10-20 ml/kg/h) of lactated Ringer's solution (RL), 10% Dextrose or Dextran 40 (D40) after surgery. 1) In the groups transfused with maintenance dose or large volumes of RL, or large volumes of D40 after 80% and 70% hepatectomy in normal dogs and 40% hepatectomy in DMNA-induced cirrhotic dogs, the extravascular lung water (EVLW) increased with a high incidence of the development of lung edema. On the other hand, in the groups transfused with maintenance dose or large volumes of 10% Dextrose, or maintenance dose of D40, EVLW did not increase, thus preventing the development of lung edema. 2) The lower the functional reserve of the remaining liver and reticuloendothelial function, the more the volume of EVLW increased. The increments in plasma endotoxin titers through the spill over phenomenon, due to the decline of reticuloendothelial function after hepatectomy, caused an increase in the permeability of lung capillaries. Moreover, the decrease of colloid hydrostatic pressure gradient (CHPG) also caused an increase in EVLW. It is clear that both the permeability of lung capillaries and CHPG contribute to the development of lung edema after hepatectomy.
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PMID:[Studies on adequate components and amounts of transfusion solution after hepatectomy from the viewpoint of the development of lung edema]. 343 40


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