Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ruminal administration of 3-methylindole in goats severe pulmonary edema and respiratory distress. Electron microscopic studies of lungs reveal extensive degeneration and necrosis of alveolar membranous pneumocytes and bronchiolar epithelium. The necrosis of the pneumocytes is followed by proliferation of granular pneumocytes, which repopulate the alveolar basal lamina scaffold. 3-Methylindole may also induce proliferation of smooth endoplasmic reticulum in the remaining membranous pneumocytes and nonciliated columnar cells, indicating that these two cell types are involved in the xenobiotic function of the lung. The results suggest that 3-methylindole in cigarette smoke may play an important role in the pathogenesis of small airway disease and emphysema, and that patients with severe liver diseases or portocaval shunt may be predisposed to diffuse alveolar damage by 3-methylindole produced in the intestinal tract.
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PMID:3-methylindole-induced pulmonary injury in goats. 86 17

1 Rapid intravenous injection of 3-methylindole (3-MI) was shown to induce an anaphylactoid-like reaction in calves. 2 This was suggested by the reduction in response to a repeat dose of 3-MI, by the reduction of effects in the presence of antagonists to the putative mediators of anaphylaxis in cattle and by the production of signs similar to those seen in experimentally induced bovine anaphylaxis. 3 The plasma half-life of 3-MI was short (14.4 min) and, since absorption of 3-MI from the rumen is known to be slow, the extent of formation of 3-MI from L-tryptophan in the rumen would have to be substantial if 3-MI is to be considered the causative agent of 'fog fever', an acute respiratory distress syndrome seen in cattle.
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PMID:Effects of 3-methylindole in cattle. 92 56

The effects of intraruminal administration of 3-methylindole (3MI; skatole) were determined in goats. The 3MI was given to 4 goats at the dose level of 0.3 g/kg of body weight, to 2 goats at 0.2 g/kg, and to 2 goats at 0.1 g/kg; 3 nontreated goats were used as controls. Clinical signs of acute progressive respiratory tract disease were seen in all treated goats. Goats given the largest dose of 3MI (0.3 g/kg) died between 5 and 11 hours after treatment; those given smaller doses (0.2 and 0.1 g/kg) died between 79 and 92 hours. Increased plasma concentrations of 3MI were detected in goats give 0.1 or 0.2 g/kg within 3 hours after administration. By 24 and 36 hours, the concentrations of 3MI in the plasma decreased to low or nondetectable amounts and remained low for the duration of the experiment. Clinical signs of respiratory distress in the goats progressed after 3MI had been cleared from the plasma. Diffuse pulmonary edema and hydrothorax were extensive in goats which died early in the course of the experimentally induced disease. In goats which died at later stages, the lungs were firm and had less watery transudate. Temporal variations in the nature of pulmonic changes were even more obvious by microscopic examination. Diffuse pulmonary edema was the predominant early change. Small foci of emphysema were apparently caused by overdistention of some clusters of alveoli. Marked septal thickening and proliferation of alveolar cells were the prominent changes in goats which died between 79 and 92 hours after treatment. Incubation of L-tryptophan with caprine ruminal fluid resulted in formation of indoleacetic acid, indole, and 3MI. Similar incubations did not convert indoleacetic acid to 3MI. Control incubations showed 3MI as a fermentation metabolite, indicating it exists in caprine ruminal fluid in vivo. Results demonstrated that goats are susceptible to intraruminal administration of 3MI. The transitory appearance of 3MI in the plasma associated with progressive respiratory tract disease was similar to observations in cattle give 3MI. Clinical signs and lesions seen at necropsy were qualitatively similar to those reported in cattle given tryptophan and indoleacetic acid.
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PMID:Induction of pulmonary edema and emphysema in goats by intraruminal administration of 3-methylindole. 93 87

Interstitial pneumonias comprise a significant proportion of cattle respiratory diseases. Known by different names, such as acute bovine pulmonary emphysema and edema (ABPE), fog fever, atypical interstitial pneumonia (AIP) and cow asthma, the condition seems to occur predominantly in late summer or fall. However, depending on the etiology, cases have occurred throughout the year. Interstitial pneumonia often begins with acute respiratory distress in animals that were clinically normal 12 hr earlier. Animals are observed breathing very rapid and shallow with their mouths open. If disturbed, death may occur rapidly from hypoxia. Causes of interstitial pneumonia are quite varied ranging from parasitic, viral and bacterial to toxic. Toxic agents constitute the most economically important cause of this condition in cattle. The primary toxin is the amino acid L-tryptophan in lush pasture grasses, a compound which is converted to 3-methylindole by rumen microorganisms. Other leading toxic causes of interstitial pneumonia are perilla mint and moldy sweet potatoes. Although treatments are mainly symptomatic and ineffective, preventive measures will reduce the occurrence of interstitial pneumonia. Prevention consists of denying animals exposure to know pneumotoxic agents, eliminating certain rumen microflora that break down the toxic compounds to reactive metabolites, and supplying ample good forage so that cattle will not as likely consume toxic plants.
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PMID:A review of interstitial pneumonia in cattle. 266 72

3-methylindole (3-MI) dissolved in the lipophilic carrier Cremophore EL was administered intraperitoneally to male, twelve-week-old Sprague-Dawley rats. Gross and histopathologic changes in the lungs were studied using light microscopy at three time-periods following administration: 16, 24, and 46 hours. Both 3-MI and Cremophore caused changes in bronchiolar epithelium at 16 hours. By 46 hours, Cremophore-injected rats showed no effects of the carrier; whereas, 3-MI rats showed severe lung changes characterized by airway epithelial and pulmonary vascular endothelial necrosis and sloughing, cellular infiltration by lymphocytes and macrophages, perivascular edema, alveolar edema, and lymph stasis. Grossly, the controls showed no effect of the carrier and none died during the studies. In contrast, 3-MI injected rats quickly became lethargic and displayed tachypnea, anorexia, and progressive respiratory distress. Two of five 3-MI rats in the final group died just prior to 46 hours. All of this group had grossly congested lungs and marked pleural effusion. The lesions and time course showed similarities to those observed in ruminants and mice. We conclude that 3-MI in Cremophore causes an acute progressive pneumonitis in rats and suggest that the rats may be a suitable model for 3-MI-induced and similar toxic lung diseases in domestic animals and people.
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PMID:Pulmonary changes in rats following administration of 3-methylindole in cremophore EL. 298 Feb 17

In 5 Friesian calves given 3-methylindole (3-MI) (100 mg/kg once a week for 8 weeks, except calf 4, given a 50 mg/kg dose on weeks 3 to 8), pulmonary function (PF) values and arterial blood gas tensions (PaO2 and PaCO2) were measured 24 hours after dosing was done and were correlated with clinical, biochemical, and pathologic changes. Three of the calves (No. 1, 2, and 3) showed acute respiratory distress syndrome 24 hours after the first 3-MI treatment, with a large increase in respiratory frequency, minute viscous work, and PaCO2 and a large decrease in tidal volume, dynamic lung compliance, and PaCO2. They died 36, 38, and 84 hours after dosing. Pulmonary function changes were compatible with the severe pulmonary edema and alveolar damage observed at necropsy. The 2 other calves, after they were given the 1st dose, showed only subacute respiratory distress syndrome with less severe changes in PF values recorded at 24 hours. Furthermore, they became progressively more tolerant to the 2nd, 3rd, and 4th weekly treatments, and showed base-line PF values after the 5th weekly treatment. Pathologic changes were not observed in lung biopsy material from these 2 animals at 2 and at 12 weeks after the 8th (or last) 3-MI treatment.
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PMID:Pathophysiologic study of 3-methylindole-induced pulmonary toxicosis in immature cattle. 403 88

The involvement of melengestrol acetate (MGA) in susceptibility to developing pulmonary edema and emphysema following oral administration of 3-methylindole (3MI) was investigated using 10 Suffolk ewes receiving 0 or 0.15 mg of MGA daily (n = 5). Blood, urine and ruminal fluid were collected immediately prior to 3MI dosing (0.2 g/kg BW) and 1, 2, 3, 4, 5, 6, 12 and 24 h (blood); 3, 6, 9, 12 and 15 h (urine) and 1, 2, 3 and 12 h (ruminal fluid) afterward. Ewes receiving MGA experienced earlier (P < 0.05) onset of respiratory distress than the control ewes (2.5 vs 4 h), and upon euthanasia at 96 h, their lung weight relative to body weight tended (P < 0.10) to be lower. Ruminal 3MI concentrations did not differ between treatments (P > 0.05). Ewes receiving MGA had higher (P < 0.05) concentrations of 3MI metabolites in plasma prior to dosing than did control ewes, and these values tended to remain higher throughout the sampling period. Immunoreactivity assays indicated more pneumotoxin present in the lungs of MGA-treated ewes than controls. Lung damage was apparently more acute and accelerated in the MGA-treated ewes than in the controls. Urinary 3MI mercapturate concentrations differed (control > MGA-treated, P < 0.05) at 9, 12, and 15 h, but this difference was not apparent when urinary production (as estimated by creatinine concentration) was considered. The implications of these findings for MGA-treated feedlot heifers are currently under investigation.
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PMID:Effect of melengestrol acetate on development of 3-methylindole-induced pulmonary edema and emphysema in sheep. 979 92