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

We hypothesized that in unilateral lung injury, bilateral hypoxic ventilation would induce vasoconstriction in the normal lung, redirect blood flow to the injured lung, and cause enhanced edema formation. Unilateral left lung injury was induced by intrabronchial instillation of 1.5 ml/kg of 0.1 N HCl. After HCl injury, blood flow to the injured left lung decreased progressively from 0.70 +/- 0.04 to 0.37 +/- 0.05 l/min and percent of flow to the injured left lung (QL/QT) decreased from 37.7 +/- 2.2 to 23.6 +/- 2.2% at 240 min. Exposure to hypoxia (12% O2) for three 10-min episodes did not affect QL/QT in normal animals, but after unilateral HCl injury, it caused blood flow to the injured left lung to increase significantly. A concomitant decrease in blood flow occurred to the noninjured right lung, resulting in a significant increase in QL/QT. The enhanced blood flow to the injured lung was associated with a significant increase in the wet-to-dry lung weight ratio in the dependent regions of the injured lung. These findings demonstrate that in unilateral HCl-induced lung injury, transient hypoxia can enhance blood flow to the areas of injury and increase lung edema formation.
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PMID:Hypoxia enhances unilateral lung injury by increasing blood flow to the injured lung. 343 82

Chlorphentermine HCl (CP) was used to induce preexisting alveolar alterations resembling a pulmonary lipidosis in mice to study these effects on the severity and duration of nitrogen dioxide (NO2) toxicity. Results indicated that a daily dose of 120 mg/kg for 14 days produced consistent histopathologic changes characterized by an accumulation of large foamy macrophages. Male Swiss-Webster mice were divided into a control and three treatment groups. Group 1 received 120 mg/kg CP po daily for 2 weeks followed by exposure to air for 48 hr. Group 2 received 20 ppm NO2 for 48 hr via whole-body inhalation, and group 3 received 120 mg/kg CP daily for 2 weeks followed by 20 ppm NO2 for 48 hr. The fourth group served as a nontreated control and received water in place of CP and air in place of NO2. All groups were compared by morphologic evaluation of pulmonary tissues at the light and electron microscopic levels at Days 0, 1, 3, 5, and 7 after the 48-hr exposure to air or NO2. In a second experiment using the same treatment groups, thin-section light microscopy was used to count the number of type I and type II cells and macrophages. NO2 exposure alone caused deaths in 20.8 and 18.5% of the mice in the two studies, but no deaths were seen in the combination groups from both experiments. Histopathologic evaluation showed a typical cellular response to the NO2 exposure, but differences were noted between the two groups receiving NO2 on this treatment. There was increased type II cell hyperplasia and terminal bronchiolitis on Days 0 and 1 but less on Days 3 to 7 in the combination group compared to the NO2 alone group. CP treatment prior to NO2 exposure caused less terminal bronchiolar epithelial hyperplasia and less pulmonary edema than was seen in the NO2 along group. The CP treatment appeared to protect against the lethal effects of NO2 at the concentration and time of exposure used and altered the cellular repair mechanism that occurs in response to NO2 toxicity. CP treatment prior to NO2 exposure caused significantly less loss of type I cells and less increase in type II cells due to NO2 damage. The combination treatment also caused an increase in macrophages greater than that seen in either individual treatment, and this number remained increased through 5 days post-NO2 exposure, whereas the NO2 alone caused a steady increase in macrophages following the exposure until Day 3.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of chlorphentermine pretreatment on the toxicity of nitrogen dioxide in mice. 362 64

Previous studies have suggested that prostaglandin synthesis inhibition might alter lung water accumulation in low pressure pulmonary edema. Therefore we studied the effects of indomethacin administration on edema formation, hemodynamics, and gas exchange in canine acid aspiration. Fourteen pentobarbital anesthetized dogs received 1 ml/kg of 0.1 N HCl intratracheally and then 7 received indomethacin (5 mg/kg) and 7 served as time controls. Lung liquid was measured in vivo by a double indicator technique and at the end of the experiment by gravimetric determinations. Following HCl administration, venous admixture (Qva/Qt) increased in both groups. Over the succeeding 4 h Qva/Qt decreased after indomethacin administration by 4.1 +/- 14.2%, but increased in the control group by 10.9 +/- 11.5% (P less than 0.05). Cardiac index remained constant in the control group but decreased after indomethacin from 232 +/- 89 ml X kg-1 X min-1 to 167 +/- 75 ml X kg-1 X min-1. Lung liquid accumulation, however, was similar between both groups. We believe that the changes in Qva/Qt associated with indomethacin can be explained by the known observations that decreases in cardiac output are associated with decreases in intrapulmonary shunt.
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PMID:The effects of indomethacin on edema and gas exchange in canine acid aspiration. 362 6

A case of fatal suicidal ingestion of "Super Blue (Gun Blue)" (gun-blueing) is presented. Post-mortem examination of the patient revealed pulmonary edema with pleural effusion and congestion of the kidney. Necrosis of proximal tubules was found in the kidney by histological examination. "Super Blue" contains 4% selenious acid and 2.5% cupric sulfate in HCl. Levels of selenium and copper in tissues of the toxic case and normal individuals were determined. The selenium levels of tissues of the patient were 9-90-fold higher than that of normal subjects, whereas concentrations of copper were about 2-fold compared to that of control levels. The highest levels of selenium in the tissues of the patient were found in the lung, kidney and stomach contents.
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PMID:An autopsy case of acute selenium (selenious acid) poisoning and selenium levels in human tissues. 374 7

Oleic acid causes pulmonary edema by increasing capillary endothelial permeability, although the mechanism of this action is uncertain. We tested the hypothesis that the damage is an oxidant injury initiated by oleic acid, using isolated blood-perfused canine lung lobes. The lobes were dilated with papaverine and perfused in zone III with a constant airway pressure of 3 cmH2O. Changes in isogravimetric capillary pressure (Pc,i) and capillary filtration coefficient (Kf,C) were used as indices of alterations in microvascular permeability in lungs treated with silicone fluid (n = 3), oleic acid (n = 11), oleic acid after pretreatment with the antioxidants promethazine HCl (n = 11) or N,N'-diphenyl-p-phenylenediamine (DPPD; n = 4), or oleic acid following pretreatment with methylprednisolone (n = 4). Kf,C averaged 0.21 +/- 0.02 ml X min-1 X cmH2O-1 X 100 g-1 in control and increased to 0.55 +/- 0.05 and 0.47 +/- 0.05 when measured 20 and 180 min after the administration of oleic acid. When oleic acid was infused into lungs pretreated with promethazine, Kf,C increased to only 0.38 +/- 0.05 ml X min-1 X cmH2O-1 X 100 g-1 after 20 min and had returned to control levels by 180 min. Pretreatment with DPPD, but not methylprednisolone, similarly attenuated the increase in Kf,C following oleic acid. Silicone fluid had no effect on Kf,C. That oleic acid increases vascular permeability was also evidenced by a fall (P less than 0.05) in Pc,i from control when measured at 180 min in every group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Promethazine or DPPD pretreatment attenuates oleic acid-induced injury in isolated canine lungs. 403 May 77

To determine the effect of the type of lung injury on the thermodilution estimation of extravascular lung water, we produced pulmonary edema in 25 anesthetized dogs by injection of alloxan or alpha-naphthylthiourea (ANTU) into the pulmonary circulation or by instillation of hydrochloric acid (HCI) into the airway. HCl injury was bilateral, unilateral with tidal volume equal in each lung, or unilateral with equal airway pressure. Extravascular thermal volume (ETV) was measured at base line and 4 h after lung injury, and the final measurement was compared with the postmortem determination of extravascular lung mass (ELM). In 11 of 15 animals with HCl injury final ETV was less than the base-line measurement. The ratio of final ETV to ELM for all HCl animal (group I) averaged 0.31 +/- 0.14, which was different from the value for animals with alloxan or ANTU injury (group II), 1.04 +/- 0.14 (P less than 0.01). Extravascular lung water per gram of blood-free dry tissue was not different for the two groups (8.1 +/- 1.2 and 8.7 +/- 2.6 for I and II, respectively), indicating equally severe lung injury; however, shunt fraction was less in group I (P less than 0.01). ETV/ELM correlated with the shunt fraction for group I (r = 0.70) but not for group II (r = 0.32). These findings indicate that ETV underestimates lung water after HCl injury due to the redistribution of pulmonary blood flow away from edematous areas.
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PMID:Type of lung injury influences the thermal-dye estimation of extravascular lung water. 643 8

The possible value of albumin in a rabbit model of the acid aspiration syndrome was studied. Hydrochloric acid was instilled into the respiratory tracts of three groups of rabbits: Group A received a high intravenous dose of human albumin (1.5 gm/kg body weight); Group B (control) was given Hartmann's solution, and Group C a low dose of albumin (0.25 gm/kg body weight). The total amount of intravenous fluids was identical in all groups. Serum and pulmonary edema fluid (PEF) concentrations of total protein were highest in Group A. Simultaneous concentration gradients between serum and PEF for total protein, human and rabbit albumin, and globulin fractions were not statistically different in the three groups. In Group A, PEF appeared first and PaO2, static compliance, and hematocrit decreased significantly more than those of the two other groups. Survival of animals in Group C was highest. An additional Group (D) of rabbits received the same high dose of albumin without acid aspiration. In Group D hematocrit decreased while serum total protein and pulmonary function remained unchanged. It seems that a high dose of albumin causes a further deterioration of lung function following acid aspiration because of extravasation into the interstitial space. The administration of low doses of albumin was not different than Hartmann's solution, but led to the best survival in our model.
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PMID:Intravenous albumin administration in acid aspiration syndrome in rabbits. 682 96

Experimental aspiration pneumonia induced in the isolated perfused ventilated canine pulmonary lobe by the intrabronchial instillation of hydrochloric acid is characterized by pulmonary edema, intrapulmonary shunting, and loss of lung compliance. In addition, pulmonary artery pressure increases. In an attempt to modify the injury response, we restricted the increase in pulmonary artery pressure in the isolated lobe model by administering vasodilator drugs. In control lobes perfused for 4 hours there was minimal weight gain (14 gm), pulmonary artery pressure remained stable (13 mm Hg), and intrapulmonary shunting did not occur. Following intrabronchial instillation of 0.2 ml of 0.1N HCl/gm of lobe weight, lobe weight tripled (183 gm), pulmonary artery pressure (20 mm Hg) was significantly increased, and significant intrapulmonary shunting (32%) developed. When sodium nitroprusside (2 micrograms/min/kg of dog body weight) was infused into the pulmonary artery 3 minutes after HCl instillation, the pulmonary artery pressure was significantly reduced (13 mm Hg) compared to that in untreated acid lobes. This was accompanied by a significant reduction in mean weight gain (100 gm) and intrapulmonary shunting (15%) compared to untreated acid lobes. Similarly, when isoproterenol (0.04 micrograms/min/kg dog body weight) was infused into the pulmonary artery following acid instillation, the pulmonary artery pressure (12.5 mm Hg) was significantly reduced compared to that in untreated acid lobes. This was also accompanied by a significant reduction in weight gain (60 gm) and intrapulmonary shunting (6%) compared to untreated acid lobes. These data demonstrate that the increase in pulmonary artery pressure following acid injury can be lowered pharmacologically and that a significant decrease in injury response follows. This suggests that the magnitude of the injury response is in part a function of pulmonary artery pressure.
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PMID:Aspiration pneumonia: treatment with pulmonary vasodilators. 685 18

The effects of acid aspiration on lung mechanics, gas exchange, haemodynamics and lung water, and their modification by nebulized dexamethasone were studied in 10 dogs. Each dog received 0.1 N HCl pH of 1.0 (15 ml/l vital capacity), instilled down the tracheal tube. PEEP 0.98 kPa (10 cm H2O) was introduced 20 minutes after aspiration and was continued until the completion of experiment. Treated animals (N = 5) received dexamethasone 5 mg . kg-1 by continuous nebulization over a two hour period starting 20 minutes after aspiration. Untreated (N = 5) animals received nebulized saline. Measurements were taken before aspiration and at 20 minutes 2.5 and 5.0 hours after aspiration. Red blood cells labelled with 51Cr were injected before sacrifice. After sacrifice multiple lung samples were taken for measurement of pulmonary extravascular water (PEW) by the gravimetric technique. Acid aspiration caused significant changes in lung volumes, PaO2, and intrapulmonary shunt. Pulmonary extravascular water was 6.16 +/- 0.93 ml/g dry tissue in treated and 6.47 +/- 0.60 ml/g dry tissue in untreated animals. These results indicate the presence of severe pulmonary oedema. There were no significant differences in any measured parameter between treated and untreated animals. We conclude that nebulized dexamethasone is of no value in treatment of the acute changes induced by acid aspiration.
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PMID:The effect of inhalation of nebulized steroid on the acid aspiration syndrome. 728 86

The acute inhalation LC50 of oxalyl chloride was determined in rats following a one-hour exposure. Four groups of 10 animals per group were exposed to a concentration range of 462-2233 ppm. One set of six animals was exposed to a concentration of oxalyl chloride of 1232 ppm for one hour to evaluate the histopathological change to the lungs. The LC50 is 1840 ppm with the 95% confidence interval between 1531 ppm and 2210 ppm. Microscopically, the lungs from the treated animals exhibited acute bronchiolitis, exudate within the alveoli, and congestion. Pulmonary edema appears to contribute significantly to mortality produced by oxalyl chloride. A comparison of the acute one-hour LC50 of oxalyl chloride to that of hydrogen chloride, phosgene, phosphorus oxychloride, boron trichloride, and chlorine indicates that it shares a comparable degree of acute toxicity to hydrogen chloride and is significantly less toxic via inhalation than the latter four chemicals.
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PMID:Acute inhalation toxicology of oxalyl chloride. 787 5


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