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

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

3-Methylindole (3MI), a ruminal fermentation product of tryptophan, is the causative agent in the development of acute bovine pulmonary edema (ABPE). The disease is dependent on the activation of 3MI by mixed function oxidases (MFO). Electron micrographs have revealed that the lamellar bodies of the type II cells are disrupted in structure and contain neutral lipids (NL) instead of surfactant phospholipids (PL). Goat lung slices were used to investigate the changes in PL metabolism induced by 3MI. Eighteen slices were cut from each lung and divided into control, 3MI (0.57 mM), and indole (0.57 mM) groups. After a 3-hr pretreatment with these compounds, the slices were incubated with [14C]acetate. The lipids were extracted and separated. 3MI inhibited the incorporation of [14C]acetate into all of the PL studied, but had little effect on its incorporation into NL. Indole displays the same effects on membranes as 3MI, but is not activated by the MFO system and does not induce lung injury. Indole pretreatment had little effect on acetate incorporation in any of the lipid fractions. These results indicate that metabolism of 3MI in lung slices is responsible for the depression of PL synthesis in vitro. Increasing the level of unlabeled choline in the medium from 10 microM to 10 microM had no effect on the depression of [14C]acetate incorporation into phosphatidylcholine (PC). This suggests that choline uptake is not limiting the synthesis of PC in the 3MI-treated lung slices.
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PMID:The effect of 3-methylindole on phospholipid synthesis in goat lung tissue slices. 669 67

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

The identification of plasma markers of the course of the acute respiratory distress syndrome (ARDS) is needed to improve its treatment and to further advance the development of new therapeutic agents. The status of markers of lung injury in ARDS is reviewed and some new potential markers are proposed. This study focused on plasma amino acids, related amino compounds, and catecholamine levels during the acute phase of endotoxin-induced lung injury in 8 sheep characterized by the onset of pulmonary edema caused by increased microvascular permeability. A number of significant changes from baseline values were found. During the sixth hour of a 12-hour period of endotoxin infusion, norepinephrine, epinephrine, and alanine levels increased whereas the isoleucine level decreased. During the sixth hour of the immediate postendotoxin period, the taurine level increased while the levels of arginine, citrulline, glycine, isoleucine, methionine, ornithine, serine, threonine, and tryptophan decreased. These findings are compared with prior studies in human subjects detailing the amino acid profile characteristic of advanced sepsis. We conclude that the present profile of catecholamine and amino acid changes during endotoxemia in sheep deserves further study in human subjects to determine its significance as a marker of the early stage of ARDS.
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PMID:A profile of amino acid and catecholamine levels during endotoxin-induced acute lung injury in sheep: searching for potential markers of the acute respiratory distress syndrome. 896 Jun 37

Indole and 3-methylindole (skatole) are odor pollutants in livestock waste, and skatole is a major component of boar taint. Skatole causes pulmonary edema and emphysema in ruminants and causes damage to lung Clara cells in animals and humans. A gas chromatographic method that originally used a nitrogen-phosphorus detector to increase sensitivity was modified resulting in an improved flame ionization detection response for indole and skatole of 236% and 207%, respectively. The improved method eliminates the large amount of indole decomposition in the injector. A 10 micro g mL(-1) spike of indole and skatole in water and swine fecal slurries resulted in recovery of 78.5% and 96% in water and 76.1% and 85.8% in fecal slurries, respectively. The effect of the addition of nitroethane and nitroethanol at 21.8 mM in swine fecal slurries was studied on the microbial production of indole and skatole. Nitroethane and nitroethanol decreased the production of skatole in swine fecal slurries at 24 h. The nitroethane effect on l-tryptophan-supplemented fecal slurries after 6 and 24 h incubation resulted in a decrease of 69.0% (P = 0.02) and 23.5% skatole production, respectively, and a decrease of 14.9% indole at 6 h, but an increase in indole production of 81.1% at 24 h.
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PMID:Effect of nitroethane and nitroethanol on the production of indole and 3-methylindole (skatole) from bacteria in swine feces by gas chromatography. 2018 70

The metabolism of 3-methylindole (3MI), a ruminal degradation product of L-tryptophan, results in acute bovine pulmonary edema and emphysema. The effect of feeding an energy or protein supplement containing monensin on ruminal 3MI formation in pastured beef cattle was investigated. A luxuriant pasture of orchard grass was established in a field that was seeded 1 year before the start of the grazing period. This 4-ha pasture was cut, fertilized, divided into 2 equal plots, and then irrigated during a 22-day growth period. All cows were fed a restricted quantity of low-quality alfalfa hay for 33 days before the grazing period. Two experiments were conducted, using 38 cows (30 of the cows were used in experiment I and all 38 cows were used in experiment II). Cows in each experiment were randomly allotted to 2 groups. One group was designated in each experiment as the control group. The control group for experiment I was fed an energy supplement. The control group for experiment II was fed a protein supplement. The 2nd group in each experiment was given the same supplement as the respective control group with 200 mg of monensin added/! kg of feed. Supplements were fed on days - 1, 0, 1, 2, 3, 4, 5, 6, and 7 of each experimental period. Supplements were fed twice daily to provide 1 kg of supplement/cow. Cows were given access to orchard grass pasture on day 0 of each experiment. Ruminal fluid was collected daily for analysis of 3MI, indole, and volatile fatty acids. Ruminal fluid pH was recorded immediately after collection. Ruminal pH of all cows decreased from 7.3 to 6.2 during the first few days of grazing the orchard grass. Ruminal pH then gradually increased toward neutrality by experimental day 10. Significantly (P < 0.01) higher molar percentages of pro-pionate and lower (P < 0.01) molar percentages of acetate and butyrate were observed in the 2 groups fed the supplements with added monensin. These changes in propionate and acetate remained different (P < 0.01) from those of the controls for 10 days (or 3 days after the last monensin feeding). Compared with pregrazing ruminal concentrations of 3MI, the 3MI values were elevated (P < 0.01) by day 1 in all groups, except in the monensin-treated cows of experiment I. In experiment I, 3MI concentrations were highest on experimental days 5 and 10 in control and monensin-treated cows, respectively. In experiment II, 3MI concentrations peaked on day 4 for the control cows and day 6 for the monensin-treated cows. Monensin supplementation reduced (P < 0.05) 3MI formation on days 1 through 5 in experiment I and on days 1 through 3 in experiment II. Formation of 3MI was increased in ruminal fluid of all cows after an abrupt change to the pasture forage, but the rate of 3MI production was slower, and a lower peak concentration of 3MI was reached in cows fed monensin than was observed in the controls. These results indicate that monensin administration in either an energy or protein supplement effectively reduced ruminal 3MI formation in pasture-fed cattle.
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PMID:Effect of energy or protein supplements containing monensin on ruminal 3-methylindole formation in pastured cattle. 2404 4


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