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[PMID]:21688624
[Au] Autor:Fujikawa Y; Watanabe T; Tominaga K; Fujiwara Y; Sato H; Arakawa T
[Ad] Endereço:Department of Gastroenterology, Osaka City University Graduate School of Medicine.
[Ti] Título:[Efficacy of prostaglandin derivatives and mucoprotective drugs in treatment and prevention for NSAIDs-induced ulcer].
[So] Source:Nihon Rinsho;69(6):1039-43, 2011 Jun.
[Is] ISSN:0047-1852
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Deficiency of prostaglandins (PGs) by non-steroidal anti-inflammatory drugs (NSAIDs) causes a loss of gastroduodenal mucosal integrity, leading to development of ulceration. PG derivatives such as misoprostol and enprostil have been proven effective in prevention and treatment of NSAIDs-induced gastroduodenal ulcers. Although side effects such as diarrhea limit the use of PG derivatives, the efficacy of these drugs in NSAIDs-induced injuries is approximately equal to that of proton pump inhibitors. Mucoprotective drugs such as rebamipide also have been reported to be effective for prevention of NSAIDs-induced ulcers. Since misoprostol and some mucoprotective drugs can prevent NSAIDs-induced small intestinal injuries, these drugs, especially misoprostol, should be used as first-line therapy for NSAIDs-induced gastrointestinal injuries with attention paid to the side effects.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/efeitos adversos
Úlcera Péptica/induzido quimicamente
Úlcera Péptica/prevenção & controle
Prostaglandinas/uso terapêutico
[Mh] Termos MeSH secundário: Emprostila/uso terapêutico
Seres Humanos
Misoprostol/uso terapêutico
Úlcera Péptica/tratamento farmacológico
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Prostaglandins); 0E43V0BB57 (Misoprostol); J4IP5Z9DAU (Enprostil)
[Em] Mês de entrada:1107
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110622
[St] Status:MEDLINE


  2 / 160 MEDLINE  
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[PMID]:20167876
[Au] Autor:Kito Y; Suzuki H
[Ad] Endereço:Dept. of Physiology, Nagoya City Univ. Medical School, Mizuho-ku, Nagoya, Japan. y.kito@med.nagoya-cu.ac.jp
[Ti] Título:Properties of Rikkunshi-to (TJ-43)-induced relaxation of rat gastric fundus smooth muscles.
[So] Source:Am J Physiol Gastrointest Liver Physiol;298(5):G755-63, 2010 May.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The relaxant effects of Rikkunshi-to (TJ-43), a gastroprotective herbal medicine, on rat gastric fundus were investigated. Experiments were carried out using standard tension and intracellular microelectrode recording techniques. During contraction induced by enprostil (0.5 microM), a prostaglandin E(2) analog, TJ-43, produced relaxation dose dependently (0.1-5.0 mg/ml) in the rat fundic circular smooth muscle (CSM) strips. The relaxant effects of TJ-43 were not affected by tetrodotoxin or 1 H[1, 2, 4] oxadiazolo [4, 3-a] quinoxalin-1-one (10 microM), an inhibitor of soluble guanylate cyclase. TJ-43 inhibited enprostil-induced membrane depolarization. Apamin (1 microM), a blocker of small-conductance Ca(2+)-activated K(+) (SK) channel, inhibited T-43-induced membrane repolarization. TJ-43-induced relaxation was biphasic, comprising of an initial fast followed by a second slow relaxation. The fast relaxation was abolished by apamin. Application of high K(+) (29.4 mM [K(+)](o)) also abolished the fast relaxation induced by TJ-43. In diabetic Goto-Kakizaki (GK) rat fundic CSM strips, the relaxant responses of TJ-43 during enprostil-induced contraction were increased compared with control rat strips. These results indicate that TJ-43 elicited fast muscle relaxation through membrane hyperpolarization induced by the activation of SK channels; the time-dependent slow relaxation reflects an additional direct of TJ-43 on CSM in the rat gastric fundus. Because TJ-43-evoked relaxation of fundic CSM strips was more potent in diabetic GK rat than in control rat, further analysis of this herb could lead to better treatments of diabetic gastroparesis.
[Mh] Termos MeSH primário: Medicamentos de Ervas Chinesas/farmacologia
Fundo Gástrico/efeitos dos fármacos
Relaxamento Muscular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apamina/farmacologia
Emprostila/antagonistas & inibidores
Hesperidina/farmacologia
Potenciais da Membrana/efeitos dos fármacos
Potenciais da Membrana/fisiologia
Músculo Liso/efeitos dos fármacos
Oxidiazóis/farmacologia
Potássio/administração & dosagem
Pirimidinonas/farmacologia
Quinoxalinas/farmacologia
Ratos
Tiazóis/farmacologia
Verapamil/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one); 0 (Drugs, Chinese Herbal); 0 (Oxadiazoles); 0 (Pyrimidinones); 0 (Quinoxalines); 0 (Thiazoles); 0 (liu-jun-zi-tang); 24345-16-2 (Apamin); 93076-89-2 (R 59022); CJ0O37KU29 (Verapamil); E750O06Y6O (Hesperidin); J4IP5Z9DAU (Enprostil); RWP5GA015D (Potassium)
[Em] Mês de entrada:1005
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100220
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00333.2009


  3 / 160 MEDLINE  
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[PMID]:16334808
[Au] Autor:Murata H; Kawano S; Tsuji S; Tsujii M; Hori M; Kamada T; Matsuzawa Y; Katsu K; Inoue K; Kobayashi K; Mitsufuji S; Bamba T; Kawasaki H; Kajiyama G; Umegaki E; Inoue M; Saito I
[Ad] Endereço:Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Japan.
[Ti] Título:Combination of enprostil and cimetidine is more effective than cimetidine alone in treating gastric ulcer: prospective multicenter randomized controlled trial.
[So] Source:Hepatogastroenterology;52(66):1925-9, 2005 Nov-Dec.
[Is] ISSN:0172-6390
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Little is known about the clinical efficacy of co-therapy of enprostil, a prostaglandin E2 analogue, with a histamine H2-receptor antagonist. We aimed to assess the additive benefit of enprostil in combination with cimetidine for treating gastric ulcer in a prospective multicenter randomized controlled trial. METHODOLOGY: In 43 hospitals 171 intention-to-treat (ITT) patients, diagnosed as having gastric ulcer by endoscopy, were randomly allocated to receive either enprostil 25microg b.i.d. and cimetidine 400mg b.i.d. (Group E=85), or cimetidine 400mg b.i.d. alone (Group C=86) for 8 weeks. Healing was examined by endoscopy at 4 and 8 weeks. RESULTS: Per protocol (PP) analysis comprised 166 patients (E=82, C=84). Despite no significant advantage at 4 weeks (E=55.3%, C=42.2%), the combination yielded higher healing rates at 8 weeks by ITT (E=89.4%, C=68.6%; p<0.001) and PP analysis (E=92.7%, C=70.2%; p<0.001). Symptom relief rates [E, C] at 2, 4, and 8 weeks were [80.2%, 68.3%] (not significant), [97.4%, 88.3%] (p<0.05), and [95.6%, 87.0%] (p<0.05), respectively. Significant advantage was observed in the patients aged 40 or older, with solitary ulcer (>5mm in diameter), and without smoking or drinking habits. No adverse effects were critical. CONCLUSIONS: Enprostil safely and significantly augmented gastric ulcer healing and symptom relief by cimetidine.
[Mh] Termos MeSH primário: Cimetidina/administração & dosagem
Emprostila/administração & dosagem
Úlcera Gástrica/tratamento farmacológico
Úlcera Gástrica/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Relação Dose-Resposta a Droga
Esquema de Medicação
Quimioterapia Combinada
Feminino
Seguimentos
Mucosa Gástrica/patologia
Gastroscopia
Seres Humanos
Japão
Masculino
Meia-Idade
Probabilidade
Estudos Prospectivos
Recidiva
Medição de Risco
Índice de Gravidade de Doença
Estatísticas não Paramétricas
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
80061L1WGD (Cimetidine); J4IP5Z9DAU (Enprostil)
[Em] Mês de entrada:0602
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:051213
[St] Status:MEDLINE


  4 / 160 MEDLINE  
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[PMID]:15005878
[Au] Autor:Sharif NA; Xu SX
[Ad] Endereço:Molecular Pharmacology Unit, Alcon Research Ltd, South Freeway, Fort Worth, TX 76134-2099, USA. naj.sharif@alconlabs.com
[Ti] Título:Pharmacological characterization and identification of EP3 prostanoid receptor binding sites in hamster uterus homogenates.
[So] Source:J Pharm Pharmacol;56(2):197-203, 2004 Feb.
[Is] ISSN:0022-3573
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The pharmacological properties of [(3)H]-prostaglandin E(2) ([(3)H]-PGE(2)) binding to washed homogenates of hamster uterus were determined. Scatchard analysis of competition data yielded dissociation constants (K(d)s) of 30.9 +/- 5.6 nM (n = 3) and apparent receptor density (B(max)) of 25.25 +/- 1.89 pmol g(-1) wet weight tissue (74 +/- 8% specific binding). Competition studies yielded the following affinity parameters (K(i)) for various prostanoids: GR63799X = 13 4 nM; PGE(2) = 17 +/- 3 nM; sulprostone = 64 +/- 5 nM; enprostil = 67 +/- 3 nM; misoprostol = 124 +/- 15 nM; cloprostenol = 187 +/- 33 nM; carba-prostacyclin = 260 +/- 167 nM; iloprost = 555 +/- 162 nM; PGF(2 alpha) = 767 +/- 73 nM; PGD(2) > 3560 nM; fluprostenol = 11 790 +/- 2776 nM; RS93520 = 21 558 +/- 14 228 nM. These data closely matched the pharmacological profile of previously described EP(3) receptors such as in bovine corpus luteum (BCLM) and the cloned mammalian EP(3) receptors. The high correlation between the current hamster uterus pharmacology data vs the EP(3) receptor binding in BCLM (r = 0.94; P < 0.0001), vs cloned human EP(3) receptor (r = 0.94, P < 0.0001), vs the cloned mouse EP(3) receptor binding (r = 0.78; P < 0.002), vs cloned rat EP(3) receptor (r = 0.9, P < 0.0004), and vs EP(3) receptor-mediated functional responses (r = 0.72, P < 0.02) substantiated the conclusion that the hamster uterus contains EP(3) receptor binding sites.
[Mh] Termos MeSH primário: Dinoprosta/análogos & derivados
Epoprostenol/análogos & derivados
Prostaglandinas/farmacologia
Receptores de Prostaglandina E/efeitos dos fármacos
Útero/citologia
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação/efeitos dos fármacos
Compostos de Bifenilo/farmacologia
Bovinos
Cloprostenol/farmacologia
Cricetinae
Dinoprosta/farmacologia
Dinoprostona/farmacologia
Emprostila/farmacologia
Epoprostenol/farmacologia
Feminino
Hidantoínas/farmacologia
Hidrazinas/farmacologia
Iloprosta/farmacologia
Misoprostol/farmacologia
Prostaglandinas E Sintéticas/farmacologia
Prostaglandinas F Sintéticas/farmacologia
Receptores de Prostaglandina E/fisiologia
Receptores de Prostaglandina E Subtipo EP3
Trítio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biphenyl Compounds); 0 (Hydantoins); 0 (Hydrazines); 0 (PTGER3 protein, human); 0 (Prostaglandins); 0 (Prostaglandins E, Synthetic); 0 (Prostaglandins F, Synthetic); 0 (Ptger3 protein, mouse); 0 (Ptger3 protein, rat); 0 (Receptors, Prostaglandin E); 0 (Receptors, Prostaglandin E, EP3 Subtype); 0E43V0BB57 (Misoprostol); 10028-17-8 (Tritium); 106342-69-2 (GR 63799X); 120962-76-7 (ZK 118182); 123122-56-5 (AH 22921); 358S7VUE5N (fluprostenol); 4208238832 (Cloprostenol); 69552-46-1 (carboprostacyclin); 6Z5B6HVF6O (latanoprost); 75693-75-3 (BW 245C); 81443-73-4 (AH 23848); 98299-61-7 (SQ 29548); B7IN85G1HY (Dinoprost); DCR9Z582X0 (Epoprostenol); J4IP5Z9DAU (Enprostil); JED5K35YGL (Iloprost); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:0406
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040310
[St] Status:MEDLINE


  5 / 160 MEDLINE  
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[PMID]:11979878
[Au] Autor:Tominaga K; Higuchi K; Watanabe T; Uchida T; Fujiwara Y; Arakawa T
[Ad] Endereço:Department of Gastroenterology, Osaka City University Graduate Medical School.
[Ti] Título:[Role of prostaglandin analog in eradication of Helicobacter pylori].
[So] Source:Nihon Rinsho;60 Suppl 2:721-6, 2002 Feb.
[Is] ISSN:0047-1852
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Mh] Termos MeSH primário: Alprostadil/análogos & derivados
Antiulcerosos/uso terapêutico
Dinoprostona/análogos & derivados
Infecções por Helicobacter/tratamento farmacológico
Helicobacter pylori
[Mh] Termos MeSH secundário: Alprostadil/farmacologia
Alprostadil/uso terapêutico
Antiulcerosos/farmacologia
Citocinas/fisiologia
Quimioterapia Combinada
Emprostila/farmacologia
Emprostila/uso terapêutico
Infecções por Helicobacter/complicações
Seres Humanos
Misoprostol/farmacologia
Misoprostol/uso terapêutico
Úlcera Péptica/tratamento farmacológico
Úlcera Péptica/etiologia
Úlcera Péptica/prevenção & controle
Prevenção Secundária
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Ulcer Agents); 0 (Cytokines); 0E43V0BB57 (Misoprostol); F5TD010360 (Alprostadil); I4LK9LH4DJ (ornoprostil); J4IP5Z9DAU (Enprostil); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:0207
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020501
[St] Status:MEDLINE


  6 / 160 MEDLINE  
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[PMID]:11979810
[Au] Autor:Jin M; Otaka M; Watanabe S
[Ad] Endereço:First Department of Internal Medicine, Akita University School of Medicine.
[Ti] Título:[New therapeutic approaches to peptic ulcer using mucosal protective agents].
[So] Source:Nihon Rinsho;60 Suppl 2:377-81, 2002 Feb.
[Is] ISSN:0047-1852
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Mh] Termos MeSH primário: Antiulcerosos/uso terapêutico
Carnosina/análogos & derivados
Chalcona/análogos & derivados
Úlcera Péptica/tratamento farmacológico
[Mh] Termos MeSH secundário: Anti-Inflamatórios não Esteroides/efeitos adversos
Antiulcerosos/farmacologia
Bicarbonatos
Carnosina/farmacologia
Carnosina/uso terapêutico
Chalcona/farmacologia
Chalcona/uso terapêutico
Chalconas
Diterpenos/farmacologia
Diterpenos/uso terapêutico
Emprostila/farmacologia
Emprostila/uso terapêutico
Mucosa Gástrica/irrigação sanguínea
Mucosa Gástrica/fisiologia
Infecções por Helicobacter/complicações
Infecções por Helicobacter/tratamento farmacológico
Helicobacter pylori
Seres Humanos
Muco/fisiologia
Compostos Organometálicos/farmacologia
Compostos Organometálicos/uso terapêutico
Úlcera Péptica/etiologia
Úlcera Péptica/fisiopatologia
Piperidinas/farmacologia
Piperidinas/uso terapêutico
Prostaglandinas/fisiologia
Sucralfato/farmacologia
Sucralfato/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Anti-Ulcer Agents); 0 (Bicarbonates); 0 (Chalcones); 0 (Diterpenes); 0 (Organometallic Compounds); 0 (Piperidines); 0 (Poraprezinc); 0 (Prostaglandins); 2B668TJX8E (sofalcone); 54182-58-0 (Sucralfate); 5S5A2Q39HX (Chalcone); 8HO6PVN24W (Carnosine); J4IP5Z9DAU (Enprostil); S8S8451A4O (geranylgeranylacetone); W6QJX1Q00Z (troxipide)
[Em] Mês de entrada:0207
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020501
[St] Status:MEDLINE


  7 / 160 MEDLINE  
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[PMID]:11119262
[Au] Autor:Toshina K; Hirata I; Maemura K; Sasaki S; Murano M; Nitta M; Yamauchi H; Nishikawa T; Hamamoto N; Katsu K
[Ad] Endereço:Second Department of Internal Medicine, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki City, Osaka 569-8686, Japan.
[Ti] Título:Enprostil, a prostaglandin-E(2) analogue, inhibits interleukin-8 production of human colonic epithelial cell lines.
[So] Source:Scand J Immunol;52(6):570-5, 2000 Dec.
[Is] ISSN:0300-9475
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We previously reported that intracolonic administration of enprostil, a prostaglandin-E(2) (PGE(2)) analogue, had therapeutic effects on acute colitis induced in rodents by dextran sulfate sodium (DSS). In addition, production of growth-regulated gene product/cytokine-induced neutrophil chemoattractant-1 [GRO/CINC-1; an interleukin(IL)-8 like cytokine] was suppressed in the inflamed tissues. In the present study we used a human colon cancer cell line (HT-29) to investigate enprostil effects on the IL-8 production of intestinal epithelial cells stimulated by various stimulants. In a MTT assay, concentrations of enprostil >10(-5)M had cytotoxitic effects on HT-29 cells. Furthermore, 10(-6) M enprostil suppressed IL-8 production in HT-29 cells, SW620 and CaCo2 stimulated with interleukin-1 beta (IL-1 beta) or lipopolysaccharide (LPS), but did not suppress this response when cells were stimulated with tumour necrosis factor (TNF)-alpha. These results suggest that enprostil affects a point in the pathway between the IL-1 receptor or LPS receptor and nuclear factor-kappa B(NF-kappa B), without affecting the pathway between the TNF receptor and NF-kappa B, with the latter factor being required for the IL-8 gene transcription. The therapeutic effect of exogenous enprostil on DSS colitis may involve the inhibition of IL-8 production in colonic epithelial cells stimulated by IL-1 beta or LPS.
[Mh] Termos MeSH primário: Colo/efeitos dos fármacos
Dinoprostona/análogos & derivados
Emprostila/farmacologia
Interleucina-8/biossíntese
Mucosa Intestinal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Colite Ulcerativa/tratamento farmacológico
Colite Ulcerativa/imunologia
AMP Cíclico/análise
Seres Humanos
Interleucina-1/imunologia
Interleucina-8/genética
Lipopolissacarídeos/imunologia
RNA Mensageiro/análise
RNA Neoplásico/análise
Transdução de Sinais
Células Tumorais Cultivadas
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-1); 0 (Interleukin-8); 0 (Lipopolysaccharides); 0 (RNA, Messenger); 0 (RNA, Neoplasm); 0 (Tumor Necrosis Factor-alpha); E0399OZS9N (Cyclic AMP); J4IP5Z9DAU (Enprostil); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:0101
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:001219
[St] Status:MEDLINE


  8 / 160 MEDLINE  
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[PMID]:10815645
[Au] Autor:Onizuka Y; Murase K; Furusu H; Isomoto H; Mizuta Y; Takeshima F; Makiyama K; Kohno S
[Ad] Endereço:Second Department of Internal Medicine, Nagasaki University School of Medicine, Japan.
[Ti] Título:Effect of intrarectal prostaglandin E2 analogue (enprostil) on trinitrobenzenesulphonic acid-induced colitis in rats.
[So] Source:J Int Med Res;28(1):28-35, 2000.
[Is] ISSN:0300-0605
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Prostaglandins exert a protective effect on colonic mucosa in experimentally induced colitis. This study investigated the effect of enprostil, a prostaglandin E2 (PGE2) analogue, on trinitrobenzenesulphonic acid (TNBS)-induced colitis in rats. Each rat received a rectal enema containing TNBS (30 mg), followed 24 h later by intrarectal once-daily enprostil (200 microg). Enprostil-treated and control rats were killed on day 3 (enprostil group, n = 5; control, n = 6) or day 10 (enprostil group, n = 5; control, n = 5) after TNBS treatment. The area of damaged mucosa of the colon was measured relative to the total colonic area. We also determined the macroscopic score of mucosal damage, and measured PGE2, 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) and thromboxane B2 (TXB2) concentration in portal vein blood samples. Enprostil significantly reduced both the area of damaged mucosa (including the ulcer area) and the macroscopic score after 3 days' treatment compared with control. Similarly, enprostil significantly reduced plasma concentration of PGE2, 6-keto-PGF1alpha and TXB2 during the acute phase at day 3 of treatment compared with control, but not at day 10. These results suggest that PGE2 enema may have therapeutic potential for treating patients with proctitis or left-sided colitis.
[Mh] Termos MeSH primário: Colite/patologia
Colo/efeitos dos fármacos
Emprostila/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Colite/tratamento farmacológico
Colo/metabolismo
Colo/patologia
Eicosanoides/metabolismo
Mucosa Intestinal/efeitos dos fármacos
Mucosa Intestinal/metabolismo
Mucosa Intestinal/patologia
Masculino
Ratos
Ratos Sprague-Dawley
Ácido Trinitrobenzenossulfônico/administração & dosagem
Ácido Trinitrobenzenossulfônico/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Eicosanoids); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid); J4IP5Z9DAU (Enprostil)
[Em] Mês de entrada:0109
[Cu] Atualização por classe:170214
[Lr] Data última revisão:
170214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:000518
[St] Status:MEDLINE


  9 / 160 MEDLINE  
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[PMID]:9430011
[Au] Autor:Omura N; Kashiwagi H; Aoki T; Omura K; Fukuchi Y
[Ad] Endereço:Department of Surgery (II), Jikei University School of Medicine, Tokyo, Japan.
[Ti] Título:Effects of enprostil on gastric endocrine secretion during chronic administration of lansoprazole.
[So] Source:J Gastroenterol;32(6):740-6, 1997 Dec.
[Is] ISSN:0944-1174
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:We investigated changes in the secretory kinetics of gastric endocrine cells related to the administration of lansoprazole, and the effects of enprostil on these altered kinetics. Male Wistar-derived 8-week-old rats were allotted to a control group, a lansoprazole administration group, an enprostil administration group, and a lansoprazole + enprostil administration group. Lansoprazole (30 mg/kg once a day for 4 weeks) and enprostil (10 micrograms/kg twice a day for 4 weeks) were administered into the gastric lumen with a gastric tube. At this time, blood was collected and immunohistological staining of gastric endocrine cells was conducted to investigate the secretory kinetics. Lansoprazole administration induced hypergastrinemia, increase of gastrin cells, and increase of enterochromaffin-like cells. Enprostil administration induced increase of somatostatin cells. The group administered lansoprazole + enprostil exhibited significant decreases in serum gastrin level, total gastrin cell count, and total enterochromaffin-like cell count, compared with the group administered lansoprazole alone. These findings suggest that enprostil may ameliorate the alteration in gastric endocrine secretion produced by the chronic administration of lansoprazole.
[Mh] Termos MeSH primário: Antiulcerosos/farmacologia
Emprostila/farmacologia
Omeprazol/análogos & derivados
Estômago/citologia
[Mh] Termos MeSH secundário: 2-Piridinilmetilsulfinilbenzimidazóis
Animais
Interações Medicamentosas
Emprostila/administração & dosagem
Células Enterocromafins/citologia
Células Enterocromafins/efeitos dos fármacos
Mucosa Gástrica/efeitos dos fármacos
Mucosa Gástrica/secreção
Células Secretoras de Gastrina/citologia
Células Secretoras de Gastrina/efeitos dos fármacos
Gastrinas/sangue
Imuno-Histoquímica
Lansoprazol
Masculino
Omeprazol/administração & dosagem
Omeprazol/farmacologia
Ratos
Ratos Wistar
Somatostatina/sangue
Células Secretoras de Somatostatina/citologia
Células Secretoras de Somatostatina/efeitos dos fármacos
Estômago/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-Pyridinylmethylsulfinylbenzimidazoles); 0 (Anti-Ulcer Agents); 0 (Gastrins); 0K5C5T2QPG (Lansoprazole); 51110-01-1 (Somatostatin); J4IP5Z9DAU (Enprostil); KG60484QX9 (Omeprazole)
[Em] Mês de entrada:9803
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:980116
[St] Status:MEDLINE


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[PMID]:9286243
[Au] Autor:Tari A; Hamada M; Kamiyasu T; Sumii K; Haruma K; Inoue M; Kishimoto S; Kajiyama G; Walsh JH
[Ad] Endereço:Department of Internal Medicine, Hiroshima Red Cross Hospital, Japan.
[Ti] Título:Effect of enprostil on omeprazole-induced hypergastrinemia and inhibition of gastric acid secretion in peptic ulcer patients.
[So] Source:Dig Dis Sci;42(8):1741-6, 1997 Aug.
[Is] ISSN:0163-2116
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study was performed to examine the effects of additional enprostil administration on hypergastrinemia and gastric acid suppression induced by omeprazole. Serum gastrin concentrations were measured in 10 peptic ulcer patients (six Helicobacter pylori-positive and four Helicobacter pylori-negative patients) before treatment, after two weeks of omeprazole (20 mg/day), and after two weeks of omeprazole and enprostil (50 micrograms/day). The additional acid inhibitory effect of enprostil was evaluated by 24-hr intragastric pH measurements in five healthy Helicobacter pylori-negative volunteers. After omeprazole treatment, the serum gastrin level of Helicobacter pylori-positive patients (3.5-fold of control) was markedly higher than that of Helicobacter pylori-negative patients (1.7-fold of control). Additional treatment with enprostil suppressed serum gastrin levels to 0.4-fold and 0.7-fold of omeprazole treatment levels in Helicobacter pylori-positive and Helicobacter pylori-negative patients, respectively. In healthy volunteers, median pH recorded during the nonmeal daytime interval increased significantly with additional enprostil. Thus, enprostil reduces undesirable omeprazole-induced hypergastrinemia, especially in Helicobacter pylori-positive patients, and effectively suppresses acid secretion.
[Mh] Termos MeSH primário: Antiulcerosos/administração & dosagem
Emprostila/administração & dosagem
Ácido Gástrico/secreção
Gastrinas/sangue
Infecções por Helicobacter/sangue
Omeprazol/efeitos adversos
Úlcera Péptica/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Antiulcerosos/efeitos adversos
Quimioterapia Combinada
Feminino
Determinação da Acidez Gástrica
Infecções por Helicobacter/complicações
Helicobacter pylori
Seres Humanos
Masculino
Meia-Idade
Omeprazol/administração & dosagem
Úlcera Péptica/sangue
Úlcera Péptica/complicações
Úlcera Péptica/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Ulcer Agents); 0 (Gastrins); J4IP5Z9DAU (Enprostil); KG60484QX9 (Omeprazole)
[Em] Mês de entrada:9709
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:970801
[St] Status:MEDLINE



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