Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mortality of ddK mice treated with 40 mg/kg i.p. of methamphetamine (MA) was 85% in grouped conditions (10 mice in a cage) and 3% in individually isolated conditions. This mortality was not altered by the social environments even when other mice in the cage were not treated with MA. The mortality of mice individually isolated in cages with transparent walls was significantly higher than that of completely isolated mice. Almost all neuroleptics dose-dependently antagonized the MA toxicity in grouped mice, in small doses. The antagonizing activity of clozapine was somewhat weak, and sulpiride potentiated MA toxicity. Phentolamine and propranolol antagonized the MA toxicity at higher doses than neuroleptics. Reserpine and tetrabenazine previously given to mice remarkably antagonized the MA toxicity. H44/68 (a tyrosine hydroxylase inhibitor) had a considerable effect in antagonizing the MA toxicity, but diethyldithiocarbamate, U-14, 624 and FLA 63 (dopamine-beta-hydroxylase inhibitors) prevented the MA toxicity to a lesser extent than did H44/68. Apomorphine had no effect on the MA toxicity. The present data show that the MA toxicity in grouped mice (the increase in mortality) was enhanced by the presence of other mice, and suggest that the norepinephrine neurons play an important role in promoting the MA toxicity. Neuroleptics antagonize MA toxicity probably by blocking alpha-receptors in the central nervous system.
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PMID:[Mechanism of methamphetamine toxicity in grouped mice and the effects of centrally acting drugs on its toxicity (author's transl)]. 2 32

The current study investigates the action of anxiolytics, antidepressants, neuroleptics, antipyretics, muscle relaxants, antihypertensives and naloxone in a novel animal model of anxiety, based on the evidence that mice removed last from their cage develop hyperthermia (stress-induced hyperthermia, SIH) when compared to those removed first. Alprazolam (0.15-0.6 mg/kg), chlordiazepoxide (25 mg/kg), estazolam (1 mg/kg), phenobarbital (20 mg/kg), ethanol (2 and 4 g/kg), buspirone (5 and 10 mg/kg) and prazosin (1 and 2 mg/kg), as well as repeatedly administered diazepam (5 mg/kg), inhibited SIH. In contrast, tofisopam (12.5-200 mg/kg), desipramine (15 and 30 mg/kg), amitriptyline (10 mg/kg), fluoxetine (10 and 20 mg/kg), tranylcypromine (5 and 10 mg/kg), chlorpromazine (1 and 2 mg/kg), clozapine (2 and 4 mg/kg), pimozide (0.5 and 1 mg/kg), l-sulpiride (15 and 30 mg/kg), l-propranolol (5 and 10 mg/kg), acetyl salicylic acid (200 and 400 mg/kg), indomethacin (2.5 and 5 mg/kg), verapamil (2.5 and 5 mg/kg), captopril (25 and 50 mg/kg), dantrolene (10 and 20 mg/kg), mephenesin (300 and 600 mg/kg), d-amphetamine (1 and 4 mg/kg) and naloxone (2.5 and 15 mg/kg) were inactive, as were 10 mg/kg imipramine, amitriptyline and fluoxetine injected every day for 21 days. Reserpine at high doses (1.25 and 2.5 mg/kg) but not at a lower dose (0.62 mg/kg) prevented SIH, but in this case animals showed a behavioural syndrome which could have interfered with the occurrence of the hyperthermia.
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PMID:Pharmacological validation of a novel animal model of anticipatory anxiety in mice. 197 57

Chronic pulmonary infections with Pseudomonas aeruginosa remain a serious problem in patients with cystic fibrosis. Structurally altered lung mucosa and local inflammation may impair bacterial clearance from the airways. This hypothesis was investigated in (1) the reserpinized rat, (2) proteinase-pretreated rat lungs, and (3) Type III hypersensitivity rat lung models. Reserpine treatment led to surface alterations of Type I epithelial lung cells and diminished food uptake. Significantly enhanced P. aeruginosa colony-forming units (CFU) were found in all (12 of 12) rat lungs 48 h after challenge compared to partially starved rats (p less than 0.025) or untreated rats (p less than 10(-6)). Pretreatment of normal rat lungs with elastase from polymorphonuclear leukocytes (PMN-elastase) resulted in extensive tissue damage, and 48 h after bacterial challenge the mean P. aeruginosa CFU of 12 animals was significantly higher 1.1 X 10(4) +/- 1.0 X 10(4) CFU; p less than 0.01) than in the reserpinized rat lungs. P. aeruginosa organisms were also found in PMN-elastase-treated rat lungs not challenged with bacteria (five of 12 animals), suggesting cross infection from infected animals in the same cage. In immunized rats that were challenged with aerosolized antigen (bovine serum albumin) and P. aeruginosa, bacterial CFU after 10 h were significantly higher than in nonimmune animals (p less than 0.005), and highest after 48 h when P. aeruginosa alkaline proteinase was used as the antigen (1.2 X 10(5) +/- 1.4 X 10(5) CFU). These data provide new evidence that clearance of P. aeruginosa from lung tissue is impaired after malnutrition, epithelial cell alteration, or epithelial cell damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clearance of Pseudomonas aeruginosa in different rat lung models. 314 14