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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute bovine pulmonary emphysema (ABPE) is known to occur throughout the world. The documented causes include 3-methylindole, 4-ipomeanol and perilla ketone. Although 4-ipomeanol is a phytoallexin from Fusarium solani, this is the first reported incidence of toxicity involving Fusarium semitectum. This report describes the poisoning of cattle consuming Fusarium semitectum contaminated pink half-runner bean refuse.
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PMID:Acute bovine pulmonary emphysema caused by the fungus Fusarium semitectum. 338 52

A series of in vitro and in vivo trials was conducted to determine if continuous monensin feeding for up to 56 d would reduce ruminal conversion of L-tryptophan (TRP) to 3-methylindole (3MI). Fourteen mature beef cows were adapted to a maintenance diet for 3 wk. In trial I, the sampling time to optimize 3MI production was determined. Trials II through IV were to determine the duration of efficacy of monensin on reducing 3MI concentrations in vitro and in vivo. During trials II, III and IV one-half of the cows were fed 200 mg monensin X head-1 X d-1 for 21, 36 and 55 d, respectively, while the remaining cows served as controls. All cows were fed the control diet for 21 d between each trial. Volatile fatty acid (VFA) concentrations and in vitro conversion of TRP to 3MI were determined in ruminal fluid samples collected during trials I through IV. On d 28 of trial IV, all cows were given an oral dose of .35 g TRP/kg of body weight to induce acute bovine pulmonary edema and emphysema (ABPE). Ruminal concentrations of 3MI and indole were measured at intervals for 96 h. Results of trial I demonstrated that ruminal fluid collected 15 h postfeeding produced the highest in vitro conversion of TRP to 3MI. Therefore, ruminal fluid samples were collected at that time in trials II, III and IV. In vitro conversion of TRP to 3MI was lower (P less than .01) in samples from monensin-treated cows (12.1%) compared with controls (25.6%). Monensin reduced 3MI production for 55 d, the longest time tested in these experiments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Duration of inhibition of 3-methylindole production by monensin. 397 43

A study was conducted to determine the dose of lasalocid that would effectively reduce ruminal conversion of tryptophan (TRP) to 3-methylindole (3MI) and prevent the development of acute bovine pulmonary edema and emphysema (ABPE). After adaptation to a maintenance diet for 3 wk, 20 mature beef cows were randomly divided into four groups of five cows each and fed 0, 200, 400 or 600 mg lasalocid X head-1 X d-1 in .5 kg ground barley for the 12-d experimental period. In vitro conversion of TRP to 3MI and indole by ruminal fluid and volatile fatty acid (VFA) concentrations were determined on d 0, 2, 4, 6 and 12. On d 6, an oral dose of .35 g TRP/kg body weight was given to induce ABPE, and ruminal production of 3MI and indole was determined at intervals thereafter. Formation of 3MI was sharply reduced (P less than .01) both in vitro and in vivo by lasalocid treatment at 200 mg X head-1 X d-1. Further suppression of 3MI production occurred as the lasalocid dose was increased (P less than .05). Linear (P less than .0001) and quadratic (P less than .002) components were determined for the relationship between lasalocid dose and 3MI production. Indole formation was variable, but tended to increase (P less than .05) with increasing lasalocid dose. Cows that received no lasalocid developed moderate to severe clinical signs of ABPE and three cows died of acute lung disease. Lasalocid treatment at all levels prevented ABPE. Lasalocid decreased ruminal acetate and butyrate, and increased propionate concentration (P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of 3-methylindole production and prevention of acute bovine pulmonary edema and emphysema with lasalocid. 397 44

Sixteen Holstein cattle allotted into 4 groups (4 cattle/group) were each given a single oral dosage of 0.2 g of 3-methylindole (3MI)/kg of body weight. The groups were killed at 12, 24, 48, and 72 hours, respectively, after 3MI administration. Comparison of clinical signs, pathologic pulmonary lesions, and in vitro pulmonary artery responses to pharmacologic stimuli was made between the 4 treated groups and 8 control Holstein cattle of similar age. Clinical signs of pulmonary distress first appeared 8 to 12 hours after 3MI administration. After 20 hours, clinical signs included dyspnea, moderate depression, and a marked expiratory grunt. A partial remission of these clinical signs was seen between 30 and 45 hours after 3MI administration. After remission, the cattle had clinical signs of severe dyspnea and depression and expiratory grunts were more pronounced. Pathologic pulmonary lesions, including heavy rubbery lungs, dilated interlobular septae, and subplural air bullae characteristic of pulmonary edema and interstitial emphysema were observed. The lungs of treated cattle did not collapse when the thorax was incised at necropsy. In vitro pulmonary artery strips contracted dose dependently to norepinephrine (NE). Group I tissues (12 hours after 3MI administration) responded similarly to control samples. Group II tissues (24 hours after 3MI administration) had a significant inhibition (P less than 0.05) in response to NE stimulation as compared with controls.
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PMID:Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle. 401 39

Microorganisms from rumen converted L-tryptophan and indoleacetic acid to 3-methylindole in vitro. Oral doses of 3-methylindole caused interstitial pulmonary edema and emphysema in cattle and goats. Intravenous infusion of this metabolite also induced pulmonary disease in cattle. These results demonstrate than an end product of ruminal fermentation of tryptophan can induce acute pulmonary disease in cattle and goats.
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PMID:Induction of pulmonary edema and emphysema in cattle and goats with 3-methylindole. 501 84

3-Methylindole (3MI), the main ruminal fermentation product of L-tryptophan, causes acute pulmonary edema and interstitial emphysema in ruminants. Intravenous infusion of 3MI in goats causes necrosis and sloughing of pneumocytes and bronchial epithelial cells. Previous studies indicate that a reactive metabolite or metabolites of 3MI bind covalently to tissue macromolecules in the lung and this binding is associated with the pneumotoxicity of 3MI. We undertook this autoradiographic study of 3MI covalent binding to test the hypothesis that reactive 3MI metabolite(s) bind to the lung cells susceptible to 3MI-induced injury. We infused goats with [3H]3MI and killed them either 0.5, 2 or 6 h after start of the infusion. Sections of fixed lung were extensively washed, alcohol dehydrated and embedded in plastic. Only covalently bound radioactivity remained. Silver grains were quantitated per area in the developed autoradiographs. There was a 2:1 ratio of binding to the small airway epithelium compared to the interalveolar septa in all the goats. Both ciliated and non-ciliated bronchiolar cells were labeled, as were both types I and II pneumocytes. Normal goat lung slices incubated in vitro with [3H]3MI were labeled in the same pattern. Inclusion of either of the inhibitors of cytochrome P-450, SKF-525-A or piperonyl butoxide significantly reduced this binding to both the pneumocytes and the bronchiolar cells. We consider these results supportive of our hypothesis that 3MI is metabolized to reactive intermediates by the epithelial cells of the lung, where they bind to macromolecules, which may cause cellular damage.
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PMID:Autoradiographic evidence of 3-methylindole covalent binding to pulmonary epithelial cells in the goat. 620 22

Ruminal bacteria can perform biochemical transformations on plant constituents that may affect the health of ruminant animals. Reactions carried out by ruminal bacteria on oxalates and some pyrrolizidine alkaloids include decarboxylation, hydrolysis and reduction steps. Prior exposure of ruminal bacteria to these substances increases the rate of detoxification, indicating an adaptive response by the bacteria to these substrates. The formation of toxic substances by ruminal bacteria also occurs and may involve similar reactions. Hydrolysis of cyanogenic glycosides and miserotoxins , reduction of nitrate and S-methylcysteine sulfoxide to nitrite and dimethyl disulfide can result in toxicity in ruminants. Similarly, the deamination and decarboxylation reactions associated with the degradation of tryptophan and tryosine result in the formation of 3-methylindole and p-cresol, which are toxic. Formation of 3-methylindole results from fermentation of tryptophan to indoleacetic acid, with subsequent decarboxylation of indoleacetic acid to 3-methylindole by a Lactobacillus sp. The 3-methylindole causes acute pulmonary edema and emphysema in ruminants as a result of mixed function oxidase metabolism in tissues. The 3-methylindole is also the cause of naturally-occurring acute bovine pulmonary edema and emphysema after abrupt pasture change. Inhibition of ruminal 3-methylindole formation by monensin and other antibiotics lowers ruminal 3-methylindole concentrations and prevents acute lung injury in experimental animals.
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PMID:Ruminal metabolism of plant toxins with emphasis on indolic compounds. 637 6

Indole and 3-methylindole (3MI) are ruminal metabolites of L-tryptophan (TRP) and have similar physical and chemical properties. 3-Methylindole causes acute bovine pulmonary emphysema (ABPE). The effects of indole when administered orally to cows were determined. Four mature Holstein cows were given increasing doses of 0.05, 0.1 and 0.2 g indole per kg body-weight orally at two-week intervals. The animals were killed one week after the last dose. Plasma indole concentrations peaked three house after administration at 4.5, 8.8 and 19.8 microgram per ml after the 0.05, 0.1 and 0.2 doses, respectively. Detectable concentrations of indole (more than 0.02 microgram per ml) persisted in the plasma from three to 25 hours after dosing. Packed cell volume was decreased (P less than 0.01) at 48 and 72 hours after the 0.2 g per kg dose and at 72 hours after the 0.1 g per kg dose. Plasma haemoglobin was increased (P less than 0.05) at 48 hours after the 0.2 and 0.1 g per kg doses. By 72 hours after the 0.2 g per kg dose, all cows had mild diarrhoea and haemolysis and two of the cows had haemoglobinuria. At necropsy, microscopic lesions of haemoglobinuric nephrosis were seen in all four cows. No lesions of ABPE were found in any of the animals.
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PMID:Indole toxicity in cattle. 721 Apr 36

Available evidence supports the view that acute bovine pulmonary edema and emphysema (ABPE) is related to ruminal production of 3-methylindole (3MI) from L-tryptophan (TRP). Ruminal production of 3MI is a two-step process involving the conversion of TRP to indoleacetic acid (IAA) followed by decarboxylation of IAA and 3MI. Reduction in ruminal 2MI production by the inhibition of either of these processes may prevent the onset of ABPE. A closed-system, in vitro ruminal fermentation technique was used to screen 27 compounds for their ability to reduce the conversion of TRP to 3MI. Several compounds tended to reduce 3MI production at both 25 and 5 micrograms/ml. Desoxysalinomycin, X-206, chloral hydrate, nigericin, lasalocid, monensin, narasin and salinomycin all reduced 3MI production by more than 80% at 5 micrograms/ml without reducing total VFA production. All of these compounds, except chloral hydrate, are polyether antibiotics. At least part of the inhibition due to monensin and narasin occurs at the level of TRP conversion to IAA.
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PMID:Inhibition of ruminal degradation of L-tryptophan to 3-methylindole, in vitro. 741 Feb 74

The pathogenesis of acute bovine pulmonary oedema and emphysema (ABPE) is related to the ruminal formation of 3-methylindole (3MI) from L-tryptophan (TRP), a naturally occurring amino acid and constituent of forage. The objectives of the present study were to determine whether monensin and lasalocid, both polyether antibiotics, were effective in reducing ruminal conversion of TRP to 3MI in vivo and to confirm that reduction in ruminal conversion of TRP to 3MI prevented tryptophan induced ABPE. Sixteen mature Hereford cows were assigned to one of four groups and given TRP to induce ABPE. Group 1 was given 100 mg monensin orally twice daily starting one day before and ending four days after TRP dosing. Group 2 was given 200 mg monensin once daily and group 3 was given 100 mg lasalocid twice daily. Group 4, the control, was given only TRP without further treatment. All control cows developed clinical signs of respiratory disease and lesions of ABPE; one control cow died of ABPE. Mean ruminal 3MI concentrations in control cows reached a peak of 36.4 micrograms per ml. Clinical signs of pulmonary disease appeared in two cows treated with lasalocid and one died. Mean ruminal 3MI in these animals peaked at 38.8 micrograms per ml. No clinical signs of respiratory disease were observed in any of the monensin treated cows and at necropsy there were no pulmonary lesions of ABPE. Mean ruminal 3MI concentrations in monensin treated cows did not exceed 8.9 micrograms per ml. In all groups plasma 3MI concentrations generally reflected ruminal 3MI concentrations but at lower concentrations. The results of this experiment demonstrate that reduction in ruminal 3MI formation by monensin prevents tryptophan induced ABPE.
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PMID:Prevention of tryptophan-induced acute bovine pulmonary oedema and emphysema (fog fever). 746 89


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