Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Toxicosis was induced in pregnant Holstein-Friesian heifers by giving polybrominated biphenyls a in gelatin capsules at the rate of 25 g/day. Initially, this dosage was approximately 67 mg/kg of body weight. Clinical signs were anorexia, excessive lacrimation and salivation, diarrhea, emaciation, dehydration, depression, and abortion. Fever was not evident during the experiment. Values for serum glutamic-oxalacetic transaminase, lactic dehydrogenase, blood urea nitrogen, and bilirubin were increased. Changes in packed cell volume, hemoglobin content, total erythrocyte and leukocyte counts, and differential leukocyte counts were minimal and reflected dehydration and secondary infection. The principal urine changes were decreased specific gravity and moderate proteinuria. Gross necropsy findings included dehydration; subcutaneous emphysema and hemorrhage; atrophy of the thymus; fetal death with concomitant necrosis of cotyledons; kidneys that were enlarged, pale tan to gray; thickened wall of the gallbladder; inspissated bile; edema of abomasal folds; mucoid enteritis; linear hemorrhage and edema of the rectal mucosa; and secondary pneumonia. Microscopic changes were most marked in the kidneys, gallbladder, and eyelid. In the kidney, the principal changes were extreme dilatation of collecting ducts and convoluted tubules, with epithelial degenerative changes of cloudy swelling, hydropic degeneration, and separation from the basement membrane. Common changes in the gallbladder were moderate to marked hyperplasia and cystic dilatation of the mucous glands in the lamina propria. The changes in the eyelids were characterized by hyperkeratosis, with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands. Clinical signs and lesions of toxicosis did not develop in heifers given the polybrominated biphenyls at the rate of 0.25 mg and 250 mg/day for 60 days. Initially these rates were approximately 0.00065 mg/kg and 0.65 mg/kg of body weight, respectively.
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PMID:Pathology of experimentally induced polybrominated biphenyl toxicosis in pregnant heifers. 18 92

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 rats exposed for 12 weeks to the mixture of nitric oxides (0.34--2.81 mg/m3) and chlorine (0.61--1.50 mg/m3) the following changes were found: increased methemoglobin concentration (MetHb), increased partial pressure, increased total carbon dioxide concentration (pCO2 TCO2), increased current dicarbonate concentration (AB), and increased buffer bases (BB). In addition, asparagine transferase activity (aspAT), alanine aminotransferase (A1AT), alkaline phosphatase (AP) and hepatic isoenzyme of lactic dehydrogenase (LDH5) in serum were found to be increased. Histopathological examination revealed: inflammatory lesions and edema of pulmonary parenchyma, alveolar emphysema and edema of connective tissue of palpetra derm with mastocytes. Chronic exposure to low concentrations of nitric oxides and chlorine induces, apart from local lesions in conjunctivae, pulmonary lesions leading to respiratory acidosis compensated by metabolic alkalosis, or liberation of indicatory enzymes through impaired cells.
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PMID:[Chemical hazards connected with electrochemical machining. I. Toxicity of nitric oxides and chlorine lesions in rats' parenchymatous organs]. 50 41

The liver, heart, lungs, and stomach of rats exposed to hydrogen fluoride were studied. Histological examination showed partial liver necrosis and emphysema. Using histochemical methods the effect of fluorine ions was found in: a reduction of the activity of succinic and beta-hydroxybutyric dehydrogenases in the liver, heart muscle, superficial and glandular epithelium cells, and in lamina propria of the gastric mucosa; an increase in the activity of lactate dehydrogenase in liver cells; an increase in the activity of acid phosphatase in the liver, heart muscle, bronchus epithelium, bronchioli, and interalveolar septum cells; an increase in the activity of alkaline phosphatase in the liver, lungs, and heart muscle connective tissue, and in all gastric epithelium cells. The results obtained mainly point to the inhibition of oxidative metabolism by fluoride ions.
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PMID:Studies on the toxicology of fluorine compounds. I. Histological and histochemical investigations on the liver, heart, lungs, and stomach of rats exposed to hydrogen fluoride. 261 87

The possibility of in situ isolated lung perfusion as a means of treating nonresectable pulmonary cancers unresponsive to conventional chemotherapy has been investigated. The present study has examined the biochemical and morphological effects of in situ isolated lung perfusion in dogs with doxorubicin (DOX). A dose related complication was seen in the animals following lung perfusion. Lactate dehydrogenase (LDH) activity in the perfusate increased as dose was increased, indicating tissue damage during the perfusion. Up to 7 days postperfusion, marked changes were seen in the serum protein concentrations although these were independent of doxorubicin concentrations. Serum lactate dehydrogenase showed a dose dependent increase 2 hour and 1 day after the lung perfusion. Plasma angiotensin converting enzyme activities up to 14 days postperfusion suggested that DOX produced pulmonary endothelial cell injury at higher drug doses. Histopathologic examination of the lungs from dogs receiving the highest concentrations of drug indicated that necrosis of arterial endothelia and alveolar epithelia accompanied by periarterial edema, subplural edema and emphysema of the lungs were the probable causes of acute animal mortality. The study has demonstrated that doxorubicin produces dose-dependent damage to the pulmonary tissue. However, the observed injury only appeared life-threatening at perfusate drug concentrations in excess of 20 nmol/ml. In situ lung perfusion for the treatment of unresectable pulmonary tumors may be clinically applicable.
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PMID:Pulmonary toxicity of doxorubicin administered by in situ isolated lung perfusion in dogs. 283 Sep 58

A group of 20 female albino rats was exposed to mosquito coil smoke, 8 h a day, 6 days per week, for 60 days. An additional group receiving air exposure served as control. The smoke-exposed animals had a lower body weight than the controls. Smoke-induced histopathological lesions, including an inflammation of the tracheal epithelium, atelectasis of the lung parenchyma, emphysema, increase of alveolar macrophages in the alveolar space and perivascular infiltration of polymorphonuclear cells were observed in the experimental rats. An elevation of enzyme activities of lactate dehydrogenase, glutamate pyruvate transaminase, glutamate oxoacetate transaminase and acid phosphatase were found in the serum of the smoke-exposed rats indicating the enzymes were released from the damaged tissues into the blood stream.
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PMID:Toxic effects of mosquito coil (a mosquito repellent) smoke on rats. II. Morphological changes of the respiratory system. 289 Dec 10

The effects of short-term exposure to ozone on control and elastase-induced emphysematous rats were examined to investigate whether emphysema would change the pulmonary susceptibility to oxidant air pollution. Emphysema was induced in rats after a single intratracheal instillation of 0.2 IU elastase/g body weight. Histologically, panacinar emphysema was apparent at 2, 4, 8, and 16 wk, that is, the total duration of the experiment. The diagnosis was confirmed by morphometry: the mean linear intercepts (MLI) of elastase-treated rats were significantly increased at all observation times, whereas the internal surface areas (ISA) of the elastase-treated rats were significantly decreased. In addition, pulmonary function tests provided supportive evidence for the diagnosis of emphysema. Respiratory system compliance and functional residual capacity showed a significant increase in elastase-treated rats. No differences in inspiratory capacity or in forced vital capacity between control rats and elastase-treated rats were observed. The above data are indicative for a rat model for elastase-induced emphysema. Short-term exposure to ozone of elastase-treated rats revealed panacinar emphysema, including an inflammatory response in the centroacinar region. No differences in MLI as well as in ISA between ozone-exposed rats (with or without emphysema) and their respective controls were observed. Short-term exposure to ozone induced an identical, significant increase in protein content, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, and glutathione peroxidase activities in lungs of normal and emphysematous rats. Moreover, these results strongly suggest that emphysematous rats are not more susceptible to ozone than nonemphysematous rats.
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PMID:Study of the effects of ozone in emphysematous rats. 291 30

A neonatal rat aorta smooth muscle cell culture system with a unique elastin-rich extracellular matrix was used as a model substrate for elastases. To study the susceptibility to solubilization of insoluble elastin, cultures were incubated in the presence of human neutrophil elastase (HNE) or porcine pancreatic elastase (PPE) and in the absence of serum for periods up to 45 min. Both the incubation media and cell layers were then assessed for elastin and collagen markers, total protein, and lactate dehydrogenase (LDH). Although HNE and PPE exhibited comparable activity against elastin purified from the cell layer, HNE exhibited a 6.7- to 25-fold reduction in its elastin solubilizing activity using intact cell layers as compared with the purified elastin, whereas PPE exhibited only a 1.5- to 2.5-fold reduction. This effect could not satisfactorily be explained as preferential inhibition of HNE activity in the culture system, because the amount of protein solubilized by HNE was 59% that of PPE. The mean elastin content of PPE-solubilized protein was 110% that of the elastin content of the corresponding cell layer; the value for HNE-solubilized protein was only 16%. Thus, the amount of elastin per microgram of solubilized protein for HNE was 15% that for PPE. Possible explanations for the greatly diminished elastolytic activity of HNE in the culture system include the preference of HNE for other substrates in the cell layer, the inability of HNE to penetrate sufficiently into the cell layer, and the presence of sulfated glycosaminoglycans in the vicinity of the elastin that act in an inhibitory fashion. Although there was extensive proteolytic damage to the extracellular matrix, LDH and DNA measurements indicated that little loss of cells or cell viability occurred. The observed differences in elastolytic activity of HNE and PPE in the culture system parallel the relative emphysema-inducing potency of the elastases in the hamster model of elastase-induced emphysema.
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PMID:Elastin in a neonatal rat smooth muscle cell culture has greatly decreased susceptibility to proteolysis by human neutrophil elastase. An in vitro model of elastolytic injury. 366 86

This study examined the effects of long-term experimental dysthyroidism on the enzymatic character of the costal diaphragm and selected respiratory parameters. Costal diaphragms from thyroidectomized (TX), euthyroid (EU), and hyperthyroid (HT) male albino rats were used. HT was induced by subcutaneous injections of triiodothyronine on alternate days for 6 wk. Minute ventilation was greater for the HT (70%) compared with the TX rats. The enzymatic potentials of glycolysis (28%), tricarboxylic acid cycle (30%), and fatty acid oxidation (16%) were significantly increased in the HT diaphragms, whereas the potentials were lower by a similar relative extent in the TX diaphragms. The proportion of alkali-labile fibers were greater in the TX and lower in the HT diaphragm. The shifts in heart and muscle lactate dehydrogenase isoenzyme activities were consistent with the fiber type changes. These findings show that dysthyroidism modifies the overall enzymatic capacity of the diaphragm (i.e., glycolysis, tricarboxylic acid cycle, and fatty acid oxidation) along with the proportion of alkali-labile to alkali-stable fiber types. These enzymatic changes are similar to those resulting from exercise training, tracheal banding, streptozotocin diabetes, and emphysema.
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PMID:Effect of experimental dysthyroidism on the enzymatic character of the diaphragm. 669 11

Homogenates of liver from cases of hepatic cirrhosis due to alpha 1-antitrypsin deficiency (PiZZ) alcoholism were analyzed for their content of various lysosomal enzymes. Also determined were the specific activities of lactate dehydrogenase, glutamate-oxaloacetate transaminase, glutamate-pyruvate transaminase, and creatine phosphokinase in the extracts of liver from cases of both kinds of hepatic cirrhosis: all of these activities were within the range of control values. Similarly, the specific activities of the following lysosomal hydrolases were unremarkable: acid phosphatase, beta-mannosidase, beta-fucosidase, beta-glucuronidase and beta-glucosidase. Hexosaminidase specific activity was increased twofold in livers from the cases of cirrhosis due to alpha 1-antitrypsin deficiency. The specific activity of alpha-mannosidase (measured at pH 4.5) in homogenates of livers from PiZZ individuals with cirrhosis and those with alcoholic cirrhosis was increased two- to four-fold. Chromatography of the high-speed supernatant fraction from homogenates of livers of cirrhotic and noncirrhotic individuals on columns of DEAE-cellulose resolved alpha-mannosidase activity into two components: under the conditions employed, acid pH optimum (pH 4.5) alpha-mannosidase did not bind to the resin, whereas intermediate pH optimum (pH 5.5) alpha-mannosidase could be eluted with 0.1 mol/l NaCl. Liver from one case of (PiZZ) alpha 1-antitrypsin deficiency and emphysema, without demonstrable cirrhosis, was found to contain normal levels of both acid alpha-mannosidase and intermediate alpha-mannosidase. However, cases of cirrhosis due to alpha 1-antitrypsin deficiency contained twice as much acid alpha-mannosidase and only one third to one fourth as much intermediate alpha-mannosidase as controls. The deficiency in hepatic intermediate alpha-mannosidase was also observed in 5 of 5 cases of alcoholic cirrhosis.
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PMID:Altered alpha-mannosidase isoenzymes in the liver in hepatic cirrhosis. 697 51


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