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)

A rhesus monkey (Macaca mulatta), accidentally exposed to vapors of methyl methacrylate for 22 hours was found in a comatose condition. Attempts to revive the animal were unsuccessful. Necropsy revealed a diffusely mottled liver, pulmonary edema, and atelectasis. The thoracic cavities each contained 30 ml of clear yellow fluid. Histopathologic review of the tissues showed central lobular liver necrosis, pulmonary edema, pulmonary emphysema, and atelectasis. Analysis of a blood sample obtained from the monkey 1.5 hours prior to death showed a normal hemogram, but elevated values for serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, phosphohexose isomerase, blood urea nitrogen, and serum sodium. The pathologic findings, laboratory results, and clinical history suggested a diagnosis of methyl methacrylate poisoning.
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PMID:Accidental methyl methacrylate inhalation toxicity in a rhesus monkey (Macaca mulatta). 40 81

In 18 patients, myocardial injury was estimated by mathematical analysis of the rise in plasma activity of alpha-hydroxybutyrate (alpha-HBDH) dehydrogenase as observed by multiple sampling after admission. This enzyme represents the lactate dehydrogenase isoenzymes LDH1 and LDH2. Changes in plasma volume were assessed by determining hematocrit values at the same time as the enzyme activities. Infarct size was expressed in IU/liter of plasma and in grams of heart muscle per liter of plasma (g/liter). Significant changes in plasma volume, reflected in hematocrit changes, occurred (average 12%): 10 patients without pulmonary edema showed an average change of 7%; for the group of eight patients with pulmonary edema, the change was 17%. When calculated infarct size was not correlated for plasma volume changes, a significant overestimation occurred (11.7%, range 0.7-29.7%). In the subgroup of patients with pulmonary edema the mean overestimation was 15.8%, and in patients without pulmonary edema, the mean overestimation was 8.5%. It is concluded that plasma volume changes after an acute myocardial infarction have to be taken into account when infarct size is calculated on the basis of plasma enzyme levels.
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PMID:The influence of plasma volume changes on enzymatic estimation of infarct size. 103 93

Hydrogen sulfide is an irritant and chemical asphyxiant gas that exerts its primary toxic effects on the respiratory and neurological systems. Exposure to hydrogen sulfide above a threshold value of 200-300 ppm is characterized by the sudden onset of hemorrhagic pulmonary edema. The purpose of this study was to determine whether this response is associated with changes in the surface properties of pulmonary surfactant. Bronchoalveolar lavage fluid was retrieved from the lungs of Fischer 344 rats exposed to two concentrations of hydrogen sulfide or fresh air for 4 h. Surface tension-lowering properties were assayed using a captive bubble surface tensiometer. Lung injury was assessed by histopathology and measurements of total protein and lactate dehydrogenase activity in the lavagate. Marked abnormalities in surfactant activity were demonstrated in the lavagates from rats exposed to the highest concentration (300 ppm) of hydrogen sulfide. These involved the properties of adsorption to the air-water interface and surface tension lowering under quasi-static interfacial compression. Exposure to 200 ppm hydrogen sulfide had no effect on minimum surface tension despite a significant increase in protein and lactate dehydrogenase in the lavagate. This would suggest a threshold-type response for the inhibition of surfactant activity by hydrogen sulfide. In vitro studies using normal rat surfactant showed that the abnormalities in surfactant activity were due to inhibitors in the edema fluid and not to a direct effect of sulfide on surfactant. The pathophysiological consequences of increased alveolar surface tension after hydrogen sulfide exposure may need to be considered in the clinical setting.
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PMID:Effects of hydrogen sulfide exposure on surface properties of lung surfactant. 186 74

Monocrotaline pyrrole (MCTP), a reactive electrophile, induces delayed and progressive pulmonary edema, vascular remodeling, and pulmonary hypertension after a single intravenous administration to rats. The effects of a single exposure of cultured bovine pulmonary artery endothelial cells (BEC) and bovine pulmonary artery smooth muscle cells (BSMC) to MCTP were examined. Monocrotaline pyrrole caused a dose-dependent, delayed, and progressive cell detachment and release of lactate dehydrogenase activity from monolayers of BECs but not BSMCs. Monolayers of BECs also released increased concentrations of 6-keto-prostaglandin F1 degrees, the stable metabolite of prostacyclin, as the post-treatment interval increased. Progressive and marked endothelial cell hypertrophy occurred after exposure to a nominal concentration of 5 or 50 micrograms/ml of MCTP but not after 0.5 micrograms/ml. Morphologic changes in monolayers of BSMCs were minimal, even up to 2 weeks after exposure. Ultrastructurally the hypertrophic, MCTP-treated BECs had enlarged cell profiles with enlarged nuclei. The nucleoli were prominent, occasionally multiple, and had separation of granular and fibrillar components. Cytoplasmic microtubules and perinuclear intermediate filaments were prominent in some cells, as were the golgi apparatus and endoplasmic reticulum. Degenerative changes were not prominent in cells that remained in the monolayer. Monocrotaline pyrrole inhibited proliferation of both cell types at concentrations (0.5 micrograms/ml) that were not cytotoxic. These findings indicate that MCTP induces direct, dose-dependent injury to cells in culture that is delayed and progressive, and the expression of this injury depends, in part, on the cell type.
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PMID:The effects of monocrotaline pyrrole on cultured bovine pulmonary artery endothelial and smooth muscle cells. 200 Sep 43

Escherichia coli hemolysin has been implicated as a pathogenicity factor in extraintestinal E. coli infections including sepsis. In the present study the effects of intravascular administration of hemolysin were investigated in isolated blood-free perfused rabbit lungs. Low concentrations of the toxin in the perfusate (0.05-5 hemolytic units/ml, corresponding to approximately 5-500 ng/ml), caused a dose- and time-dependent release of potassium, thromboxane A2, and prostaglandin I2, but not of lactate dehydrogenase, into the recirculating medium, as well as a dose-dependent liberation of the prostanoids into the bronchoalveolar space. These events were paralleled by a dose-dependent pulmonary hypertension, and studies with different inhibitors collectively indicated that the vasoconstrictor response was mediated predominantly by pulmonary thromboxane generation. In addition, E. coli hemolysin elicited a protracted, dose-dependent increase in the lung capillary filtration coefficient, which was independent of the prostanoid-mediated pressor response and resulted in severe pulmonary edema formation. We conclude that E. coli hemolysin can elicit thromboxane-mediated pulmonary hypertension combined with severe vascular leakage in isolated lungs in the absence of circulating inflammatory cells and humoral mediator systems, mimicking the key events in the development of acute respiratory failure in states of septicemia.
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PMID:Thromboxane-mediated hypertension and vascular leakage evoked by low doses of Escherichia coli hemolysin in rabbit lungs. 250 Apr 55

Total lactate dehydrogenase (LD; EC 1.1.1.27) activity in serum and LD isoenzymes were quantified in 190 patients with acute myocardial infarction (AMI) 24, 48, and 72 h after admission. In 90% of the 570 blood specimens an LD isoenzyme pattern typical of AMI (LD-1/LD-2 greater than 0.76) was found. The other 56 blood specimens showed an LD isoenzyme pattern atypical of AMI (LD-1/LD-2 less than 0.76). They were divided into three groups: 28 specimens with isomorphic pattern (relative increase in all five LD isoenzymes); 18 with relatively increased LD-3 proportion (greater than 35%); and 10 specimens with increased LD-5 proportion (greater than 10%). No difference was found in mean total LD activity in serum between the typical isoenzyme group and the three atypical groups. The LD isomorphic pattern was found in 60% of AMI patients complicated by cardiogenic shock. Fifty percent of AMI patients admitted with pulmonary edema showed increased LD-3 proportion and half of the patients with AMI and congestive heart failure, predominant right, demonstrated increased LD-5 proportion. We conclude that although most patients with AMI present at diagnosis with a typical LD isoenzyme pattern, it is important to recognize that some may present with atypical LD isoenzyme patterns, which may be associated with specific AMI complications.
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PMID:Atypical patterns of lactate dehydrogenase isoenzymes in acute myocardial infarction. 337 25

Neutrophils play a role in the development of pulmonary edema in many models of the adult respiratory distress syndrome, but the mechanism of their action is not completely understood. We asked whether two neutrophil secretory products, human neutrophil cationic protein (NCP) and human neutrophil elastase (HNE), would nonenzymatically alter the movement of albumin across a cultured endothelial monolayer. Both enzymes were inactivated by heating before use. HNE was additionally enzymatically inactivated with a chloromethylketone oligopeptide (CMK) inhibitor and with alpha 1-proteinase inhibitor (alpha 1-PI). Heated NCP, heated HNE, and CMK-complexed HNE all increased transendothelial albumin transfer. The cation protamine also increased albumin transfer across the endothelium and this increase was blocked by heparin. Alpha 1-PI and fetal bovine serum also prevented the cationic proteins from increasing albumin transfer. Using the release of lactate dehydrogenase as a marker of cytotoxicity, heated HNE was toxic to endothelial cells, heated NCP had only minimal toxicity, and protamine had no toxicity. Changes in endothelial cell shape with gap formation was seen after exposure to both heated HNE and heated NCP. Both the cytotoxicity associated with heated HNE and the cell shape changes associated with heated NCP and heated HNE could be blocked by heparin. These results suggest that in addition to neutrophil proteases and reactive O2 molecules, neutrophil-derived cationic proteins can directly and nonenzymatically contribute to edema formation during acute inflammation.
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PMID:Cationic neutrophil proteins increase transendothelial albumin movement. 364 23

Hyperthyroidism was diagnosed in 131 cats during a 3 1/2-year period. The cats ranged in age from 6 to 20 years; there was no breed or sex predilection. The most frequent clinical signs included weight loss, polyphagia, increased activity, polydipsia, polyuria, and vomiting. Common serum biochemical abnormalities included high values for alkaline phosphatase activity (75%), lactate dehydrogenase activity (66%), aspartate transaminase activity (66%), and alanine transaminase activity (54%). Electrocardiographic changes included tachycardia (greater than or equal to 240 beats/min) and increased R-wave amplitude in lead II (greater than or equal to 0.9 mV) in 66% and 29% of the 131 cats, respectively. Thoracic radiography in 82 cats revealed cardiomegaly in 40 (49%) of these cats; 16 cats with congestive heart failure also had pulmonary edema or pleural effusion. In 5 cats with markedly increased fecal volume, mean 48-hour fecal fat content was significantly greater than normal, with daily fat excretion 2 to 15 times the upper limit of normal. Base-line serum thyroxine concentrations were increased above normal range in all cats, whereas triiodothyronine concentrations were increased in 127 (97%) of the 131 cats. In 11 cats tested, mean thyroxine concentration did not increase significantly after thyroid-stimulating hormone administration. Mean 24-hour percentage of thyroid radioiodine uptake in 32 hyperthyroid cats was significantly higher (39.1%) than normal (9.2%). Thyroid scans, performed on 126 cats, showed enlargement and increased radionuclide accumulation in 1 thyroid lobe in 36 (29%) and both lobes in 90 (71%) of the cats.
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PMID:Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. 687 10

1. Isolated perfused rabbit lungs and cultured pulmonary endothelial cells take up radiolabeled [14C]morphine in proportion to the amount of labeled drug in the medium. 2. The accumulated label is readily released from the isolated lungs by perfusion with unlabeled morphine or naloxone, but not by perfusion with Krebs-Ringer solution, sucrose or thiopental. 3. Thiourea also enhances efflux of radioactivity, suggesting that the release is not related to interaction with specific opiate receptors. 4. Uptake of [14C]morphine by cultured rabbit or human endothelial cells is unaffected by morphine or naloxone, and the release of radioactivity is not enhanced by these agents. 5. None of the drugs used caused pulmonary edema in the isolated lung preparation, and they did not cause the release of lactic dehydrogenase from cultured endothelial cells. 6. It is concluded that morphine can be taken up by pulmonary endothelium, but it is probably not bound to specific receptors, and it does not injure the endothelial cells.
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PMID:Uptake and release of 14C-morphine by pulmonary endothelium and cultured pulmonary endothelial cells. 709 89

To investigate how mitochondrial function was affected in leukotoxin (Lx)-,9,10-epoxy-12-octadecenoate-induced lung injury, lung mitochondria were extracted from isolated perfused rat lung with or without Lx-induced edematous injury. In the lung treated with 30 mumol of Lx, the mitochondrial respiration rate in states 3 and 4 significantly decreased (without mitochondrial uncoupling) concomitantly with increased release of lactate dehydrogenase (LDH), a parameter for cellular damage, into the perfusate and decreased ATP content in the lung tissue compared with those of untreated lung. Moreover, 30 mumol of Lx resulted in significant inhibition of cytochrome-c oxidase activity (vs. vehicle control). In contrast, lower doses of Lx (10 mumol) caused lung edema and cellular damage without evidence for mitochondrial dysfunction. We also examined cellular and mitochondrial damage in hydrostatic lung edema. Such edema showed neither suppressed mitochondrial respiration nor elevated LDH activity in perfusate, although lung wet weight increased as much as it did after 30 mumol Lx treatment. Our results suggest that the ex vivo mitochondrial dysfunction is one of the secondary (vs. initial augmented permeability) but specific manifestations of toxicity of Lx, and together with the previous reports, the ex vivo damaging effect of Lx against mitochondria may be ascribed not to its direct action on mitochondria but to Lx-derived cellular mechanism(s).
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PMID:Leukotoxin, 9,10-epoxy-12-octadecenoate inhibits mitochondrial respiration of isolated perfused rat lung. 757 65


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