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  • 1
    Electronic Resource
    Electronic Resource
    The influence of chronic nicotine treatment on stress-induced gastric ulceration and emptying rate in rats (1992)
    Springer
    Cellular and molecular life sciences 48 (1992), S. 389-391 
    Details
    ISSN: 1420-9071
    Keywords: Nicotine ; cold-restraint stress ; gastric ulcers and motility
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Ten-day treatment with nicotine, (5, 25 or 50 μg/ml drinking water) dose-dependently intensified gastric ulceration induced by cold-restraint, and emptying rate. Stomach contractions produced by graded doses of bethanechol i.v. were elevated further by nicotine treatment. It is suggested that chronic nicotine administration produces hypersensitivity of the gastric muscarinic receptors; stomach hypermotility contributes to the ulcer-worsening action of the alkaloid
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01923437
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  • 2
    Electronic Resource
    Electronic Resource
    Utilization of inorganic carbon in the edible cyanobacterium Ge-Xian-Mi (Nostoc) and its role in alleviating photo-inhibition (2004)
    Oxford, UK : Blackwell Science Ltd
    Plant, cell & environment 27 (2004), S. 0 
    Details
    ISSN: 1365-3040
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: The present work investigated the inorganic carbon (Ci) uptake, fluorescence quenching and photo-inhibition of the edible cyanobacterium Ge-Xian-Mi (Nostoc) to obtain an insight into the role of CO2 concentrating mechanism (CCM) operation in alleviating photo-inhibition. Ge-Xian-Mi used HCO3– in addition to CO2 for its photosynthesis and oxygen evolution was greater than the theoretical rates of CO2 production derived from uncatalysed dehydration of HCO3–. Multiple transporters for CO2 and HCO3– operated in air-grown Ge-Xian-Mi. Na+-dependent HCO3– transport was the primary mode of active Ci uptake and contributed 53–62% of net photosynthetic activity at 250 µmol L−1 KHCO3 and pH 8.0. However, the CO2-uptake systems and Na+-independent HCO3– transport played minor roles in Ge-Xian-Mi and supported, respectively, 39 and 8% of net photosynthetic activity. The steady-state fluorescence decreased and the photochemical quenching increased in response to the transport-mediated accumulation of intracellular Ci. Inorganic carbon transport was a major factor in facilitating quenching during the initial stage and the initial rate of fluorescence quenching in the presence of iodoacetamide, an inhibitor of CO2 fixation, was 88% of control. Both the initial rate and extent of fluorescence quenching increased with increasing external dissolved inorganic carbon (DIC) and saturated at higher than 200 µmol L−1 HCO3–. The operation of the CCM in Ge-Xian-Mi served as a means of diminishing photodynamic damage by dissipating excess light energy and higher external DIC in the range of 100–10000 µmol L−1 KHCO3 was associated with more severe photo-inhibition under strong irradiance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3040.2004.01248.x
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  • 3
    Electronic Resource
    Electronic Resource
    Chronic nicotine treatment intensifies gastric ulceration by cold-restraint stress in rats (1991)
    Springer
    Inflammation research 33 (1991), S. 367-370 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nicotine 5, 25 or 50 μg/ml drinking water givenad lib for 5, 10 or 20 days, dose- and time-dependently worsened cold-restraint-induced (stress) ulceration in rat stomachs. Treatment with nicotine 5 or 25 μg/ml did not influence the number of gastric mucosal mast cells degranulated by cold and restraint; however, drinking 50 μg/ml for 10 days lowered further the mast cell count in stressed animals. During 20-day nicotine administration, the daily food intake and body weight gain, up to the 18th day when the animals were starved before experiments, were not affected by the three concentrations of the alkaloid, except that fluid consumption tended to be less only in those animals given the highest dose. The findings indicate that chronic nicotine treatment exacerbates the severity of stress-evoked ulcer formation. The ulcer-intensifying mechanism of the two lower doses of nicotine appears not to be related to additional mast cell degranulation; only the ulcerogenic action of the highest concentration includes this factor. It is unlikely that ulcer aggravation by nicotine is due to malnutrition because body weight gain and solid food intake by the alkaloid-treated rats were normal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01986587
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  • 4
    Electronic Resource
    Electronic Resource
    Nitric oxide inhibition intensifies cold-restraint induced gastric ulcers in rats (1993)
    Springer
    Cellular and molecular life sciences 49 (1993), S. 304-307 
    Details
    ISSN: 1420-9071
    Keywords: NW-nitro-l-arginine methyl ester ; nitric oxide ; cold-restraint stress ; mucosal ulcers ; mast cells ; rat stomachs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Treatment 20 min beforehand with an inhibitor of nitric oxide (NO) synthesis, NW-nitro-l-arginine methyl ester (L-NAME) (12.5, 25, 50 or 100 mg/kg, s.c.), dose-dependently intensified gastric glandular mucosal ulceration produced by cold-restraint stress. Hexamethonium (20 mg/kg) or atropine (1 mg/kg) pretreatment s.c. 20 min before stress strongly antagonised stress-evoked ulceration, as well as the ulcer-potentiating effects of L-NAME when either cholinoceptor antagonist was given concurrently with the NO inhibitor. Stress-induced mast cell degranulation was not worsened by L-NAME pretreatment. The findings suggest that NO could confer partial protection against stress-induced gastric ulcer formation; its activity is triggered off by the ulcerogenic mechanism of stress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01923407
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  • 5
    Electronic Resource
    Electronic Resource
    Influence of repeated prazosin administration on cardiovascular responses in rats and rabbits (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 66-69 
    Details
    ISSN: 1420-9071
    Keywords: Prazosin ; tolerance ; blood pressure ; rats ; rabbits
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Prazosin was injected i.v. at a dose of 50 μg/kg every 2 h for 8 h in conscious rats. Its hypotensive action significantly declined. A similar effect was also observed in rabbits pretreated with prazosin (40 μg/kg, i.v.) every 1 h for 4 h. In prazosin-treated rabbits, the total peripheral resistance became less responsive to phentolamine stimulation. Repeated prazosin administration abolished its ability to block receptors in a model of anococcygue muscle contraction after noradrenaline (NA) stimulation. The α-adrenoceptors in anococcygue muscle exhibited lower pD2 to NA and lower pA2 to prazosin in prazosin-treated rats. The results demonstrate that repeated prazosin administration reduces the effectiveness of α-adrenoceptors blockers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01922418
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  • 6
    Electronic Resource
    Electronic Resource
    Protection by recombinant human interleukin-11 against experimental TNB-induced colitis in rats (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 1625-1630 
    Details
    ISSN: 1573-2568
    Keywords: trinitrobenzene sulfonic acid ; myeloperoxidase ; colitis ; recombinant human interleukin-11 ; prostaglandin E2 ; leukotriene B4 ; thromboxane B2 ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The potential effect of recombinant human interleukin-11 (rhIL-11) on trinitrobenzene sulfonic acid (TNB) -induced colitis was investigated in rats. Intrarectal TNB (40 mg in 0.25 ml 40% ethanol) produced significant ulcerative colitis. The lesions were most severe at three days after TNB instillation, and then declined, but lesions were still observed after two weeks. TNB administration also significantly enhanced the colonic mucosal myeloperoxidase (MPO) levels, which paralleled the severity of colitis. The rhIL-11 at subcutaneous doses of 300 or 1000µg/kg daily for seven days, or 1000µg/kg for three days when given after TNB significantly decreased lesion formation in TNB-induced colitis. These treatments also significantly reduced colonic mucosal MPO levels. TNB enhanced colonic mucosal levels of PGE2, LTB4, and TxB2, but these arachidonic acid derivatives were not affected by the present rhIL-11 treatments. TNB administration for three days caused a body weight loss that returned to normal after 14 days. The rhIL-11 significantly reduced colonic lesion severity and reduced colonic fecal blood loss. Given alone, rhIL-11 did not influence body weight. It can be concluded that rhIL-11 was protective against TNB-induced colitis and reactions of colonic MPO, but that these responses were not mediated through modulation of eicosanoid metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02087911
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