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Fotocópia
[PMID]:8928090
[Au] Autor:De La Cruz JP; Moreno A; Mérida F; García Campos J; Sánchez de la Cuesta F
[Ad] Endereço:Department of Pharmacology and Therapeutics, School of Medicine, University of Malaga, Spain.
[Ti] Título:The pyrimido-pyrimidine derivatives, dipyridamole, mopidamol and RA-642, prevent from retinal vascular defects in experimental diabetes mellitus.
[So] Source:Thromb Res;81(3):327-37, 1996 Feb 01.
[Is] ISSN:0049-3848
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We compared the effects of dipyridamole, RA-642, and mopidamol on platelet activity and thromboxane/prostacyclin balance in relation to the degree of retinal vascularization in a model of experimental streptozotocin-induced diabetes in rats. After 3 months, collagen-induced platelet aggregation in whole blood was 25% higher in diabetic animals than in nondiabetics. Dipyridamole inhibited 43% platelet aggregation, mopidamol 39%, and RA-642 36%. Platelet production of thromboxane B2 was 87% higher in untreated diabetic rats. Mopidamol and RA-642 produced a 46% and 41% inhibition of thromboxane B2. Dipyridamole did not inhibited thromboxane B2 synthesis. Aortic production of 6-keto-PGF1 alpha was 43% lower in untreated diabetic animals and showed no change after treatment with either mopidamol or RA-642. In contrast, dipyridamole caused a 90% increase in aortic production of prostacyclin. Computerized analysis of retinal vascularization showed that untreated diabetic rats had a 81% decrease in the area occupied by peroxidase-labelled vessels as compared with nondiabetics. Treatment with dipyridamole, mopidamol, and RA-642 caused 2.5-fold, 2.8-fold and four-fold increases, respectively, in the percentage of retinal surface occupied by peroxidase-labelled vessels. Differences in retinal vascularization between diabetic animals given RA-642 and nondiabetic controls were negligible.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Retinopatia Diabética/prevenção & controle
Dipiridamol/farmacologia
Mopidamol/farmacologia
Inibidores da Agregação de Plaquetas/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Diabetes Mellitus Experimental/complicações
Diabetes Mellitus Experimental/metabolismo
Retinopatia Diabética/metabolismo
Epoprostenol/metabolismo
Masculino
Neovascularização Patológica/prevenção & controle
Ratos
Ratos Wistar
Tromboxanos/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Platelet Aggregation Inhibitors); 0 (Pyrimidines); 0 (Thromboxanes); 4Q0IWP8B8O (Mopidamol); 54093-30-0 (RA 642); 64ALC7F90C (Dipyridamole); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:9610
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960201
[St] Status:MEDLINE


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Fotocópia
[PMID]:8863175
[Au] Autor:Ambrus JL; Stadler I; Kulaylat M; Koreshi A; Akhtar S
[Ad] Endereço:Department of Internal Medicine, University of New York.
[Ti] Título:Hemorrheologic effects of pyrimido-pyrimidine derivatives.
[So] Source:J Med;27(1-2):21-32, 1996.
[Is] ISSN:0025-7850
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A series of pyrimido-pyrimidine derivatives were tested for their effect on membrane fluidity-deformability of human red blood cells and on human platelet aggregation. These agents were also tested for their intracellular cAMP increasing activity and proliferation inhibitory activity in neoplastic cells. The order of activity was established and clinical implications discussed. Several derivatives are under study as antineoplastic agents.
[Mh] Termos MeSH primário: Hemorreologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: 3',5'-AMP Cíclico Fosfodiesterases/antagonistas & inibidores
Difosfato de Adenosina/farmacologia
Antineoplásicos/química
Antineoplásicos/farmacologia
Divisão Celular/efeitos dos fármacos
AMP Cíclico/metabolismo
Deformação Eritrocítica/efeitos dos fármacos
Seres Humanos
Melanoma/metabolismo
Estrutura Molecular
Mopidamol/farmacologia
Agregação Plaquetária/efeitos dos fármacos
Inibidores da Agregação de Plaquetas/química
Inibidores da Agregação de Plaquetas/farmacologia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Platelet Aggregation Inhibitors); 0 (Pyrimidines); 4Q0IWP8B8O (Mopidamol); 61D2G4IYVH (Adenosine Diphosphate); E0399OZS9N (Cyclic AMP); EC 3.1.4.17 (3',5'-Cyclic-AMP Phosphodiesterases)
[Em] Mês de entrada:9612
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960101
[St] Status:MEDLINE


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Fotocópia
[PMID]:8842690
[Au] Autor:De la Cruz JP; Olveira C; Gonzalez-Correa JA; Benítez A; Sánchez de la Cuesta F
[Ad] Endereço:Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain.
[Ti] Título:Inhibition of ferrous-induced lipid peroxidation by dipyridamole, RA-642 and mopidamol in human lung tissue.
[So] Source:Gen Pharmacol;27(5):855-9, 1996 Jul.
[Is] ISSN:0306-3623
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1. The in vitro production of ferrous-induced lipid peroxidation was 5.71 times higher in rat lung tissue than in human lung membranes. 2. The pyrimido-pyrimidine derivative RA-642 shows a more potent inhibition of ferrous-induced lipid peroxidation than dipyridamole; mopidamol had no effect. All the compounds showed higher anti-peroxidative effect in rat than in human lung tissue.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Dipiridamol/farmacologia
Compostos Ferrosos/antagonistas & inibidores
Peroxidação de Lipídeos/efeitos dos fármacos
Pulmão/metabolismo
Mopidamol/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Feminino
Compostos Ferrosos/farmacologia
Seres Humanos
Técnicas In Vitro
Pulmão/efeitos dos fármacos
Masculino
Malondialdeído/metabolismo
Meia-Idade
Ratos
Ratos Wistar
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
Vitamina E/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Ferrous Compounds); 0 (Pyrimidines); 0 (Thiobarbituric Acid Reactive Substances); 1406-18-4 (Vitamin E); 4Q0IWP8B8O (Mopidamol); 4Y8F71G49Q (Malondialdehyde); 54093-30-0 (RA 642); 64ALC7F90C (Dipyridamole)
[Em] Mês de entrada:9701
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960701
[St] Status:MEDLINE


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Fotocópia
[PMID]:7771466
[Au] Autor:Meehan KR; Zacharski LR; Moritz TE; Rickles FR
[Ad] Endereço:Department of Veterans Affairs Medical & Regional Office Center, White River Junction, Vermont 05009-0001, USA.
[Ti] Título:Pretreatment fibrinogen levels are associated with response to chemotherapy in patients with small cell carcinoma of the lung: Department of Veterans Affairs Cooperative Study 188.
[So] Source:Am J Hematol;49(2):143-8, 1995 Jun.
[Is] ISSN:0361-8609
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Small cell carcinoma of the lung (SCCL) responds commonly to combination chemotherapy but resistance to therapy follows. Prior reports have suggested that a relationship may exist between plasma fibrinogen levels and response to therapy in SCCL. This study was designed to determine the possible predictive value of the fibrinogen level for tumor response (chemoresistance) in SCCL. Pretreatment fibrinogen levels were correlated with outcome and response to therapy in a cohort of 119 previously untreated patients with SCCL who were admitted to VA Cooperative Study 188. Higher pretreatment fibrinogen levels at diagnosis correlated significantly with more advanced stage of disease at entry (P < 0.001) and with reduced overall survival (P = 0.030). In addition, higher pretreatment fibrinogen levels were correlated significantly with a reduced likelihood of achieving subsequent disease regression with combination chemotherapy (P = 0.005). Because several clinical trials have shown that anticoagulant therapy improves tumor response rates and survival of SCCL, we postulate that tumor cell thrombin generation not only promotes SCCL growth but may also be primarily responsible for both increased fibrinogen levels and for resistance to chemotherapy. These findings provide incentive for studies of thrombin effects on the development of multidrug resistance, and for new clinical trials of more potent and specific inhibitors of thrombin that may further improve tumor response and survival in SCCL.
[Mh] Termos MeSH primário: Carcinoma de Células Pequenas/sangue
Fibrinogênio/análise
Neoplasias Pulmonares/sangue
[Mh] Termos MeSH secundário: Carcinoma de Células Pequenas/tratamento farmacológico
Carcinoma de Células Pequenas/fisiopatologia
Estudos de Coortes
Resistência a Medicamentos
Fibrinolisina/análise
Fibrinopeptídeo A/análise
Fibrinopeptídeo B/análise
Seres Humanos
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/fisiopatologia
Mopidamol/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Análise de Regressão
Trombina/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
25422-31-5 (Fibrinopeptide A); 36204-23-6 (Fibrinopeptide B); 4Q0IWP8B8O (Mopidamol); 9001-32-5 (Fibrinogen); EC 3.4.21.5 (Thrombin); EC 3.4.21.7 (Fibrinolysin)
[Em] Mês de entrada:9507
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:950601
[St] Status:MEDLINE


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Fotocópia
[PMID]:7701482
[Au] Autor:De La Cruz JP; Villalobos MA; Palacios R; Smith-Agreda JM; Sánchez de la Cuesta F
[Ad] Endereço:Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain.
[Ti] Título:In vitro effect of mopidamol on platelet-subendothelium interaction.
[So] Source:Thromb Res;77(1):97-103, 1995 Jan 01.
[Is] ISSN:0049-3848
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Endotélio Vascular/efeitos dos fármacos
Mopidamol/farmacologia
Inibidores da Agregação de Plaquetas/farmacologia
Agregação Plaquetária/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Comunicação Celular/efeitos dos fármacos
Dipiridamol/farmacologia
Seres Humanos
Técnicas In Vitro
Masculino
Perfusão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platelet Aggregation Inhibitors); 4Q0IWP8B8O (Mopidamol); 64ALC7F90C (Dipyridamole)
[Em] Mês de entrada:9505
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:950101
[St] Status:MEDLINE


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Fotocópia
[PMID]:8304965
[Au] Autor:De La Cruz JP; Ortega G; Sánchez de la Cuesta F
[Ad] Endereço:Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain.
[Ti] Título:Differential effects of the pyrimido-pyrimidine derivatives, dipyridamole and mopidamol, on platelet and vascular cyclooxygenase activity.
[So] Source:Biochem Pharmacol;47(2):209-15, 1994 Jan 20.
[Is] ISSN:0006-2952
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The chronic administration of 10 mg/kg/day of dipyridamole to rats produced 33.7% inhibition of platelet aggregation induced with ADP and a 93% increase in 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in vascular samples, versus saline-treated rats. Mopidamol, 8.3 mg/kg/day, caused 50.6% inhibition of ADP-induced platelet aggregation, 37.6% inhibition of aggregation induced with arachidonic acid, a 47.6% decrease in serum levels of thromboxane B2 and a 23.7% increase in the vascular production of 6-keto-PGF1 alpha, versus saline-treated rats. Dipyridamole showed a higher in vitro anti-aggregating effect in whole blood (IC50 6.6 microM) than in platelet-rich plasma (PRP) (IC50 210 microM), when ADP was used as inducer, and had no effect in the presence of arachidonic acid. Mopidamol exerted a similar effect in whole blood (IC50 3.7-20 microM, depending on the inducer) and PRP (IC50 11-17.3 microM), and showed a dose-dependent inhibition of platelet aggregation and thromboxane B2 synthesis induced with arachidonic acid (IC50 16.8-22.3 microM). Mopidamol also inhibited enzymatically induced lipid peroxidation) (IC50 89 +/- 5.9 mumol/L) and had no effect on free radical-induced lipid peroxidation. The dose-dependent increase in 6-keto-PGF1 alpha in vascular samples after incubation with dipyridamole showed a negative linear correlation with inhibition of lipid peroxidation (r2 = 0.77). It is concluded that the phosphodiesterase inhibitors, dipyridamole and mopidamol, interfere in a different manner with platelet function. It seems that mopidamol may also exert a selective effect on platelet thromboxane synthesis.
[Mh] Termos MeSH primário: Plaquetas/enzimologia
Vasos Sanguíneos/enzimologia
Dipiridamol/farmacologia
Mopidamol/farmacologia
Prostaglandina-Endoperóxido Sintases/metabolismo
[Mh] Termos MeSH secundário: Animais
Inibidores de Ciclo-Oxigenase/farmacologia
Ativação Enzimática/efeitos dos fármacos
Epoprostenol/biossíntese
Seres Humanos
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Agregação Plaquetária/efeitos dos fármacos
Ratos
Ratos Wistar
Tromboxano A2/biossíntese
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclooxygenase Inhibitors); 4Q0IWP8B8O (Mopidamol); 57576-52-0 (Thromboxane A2); 64ALC7F90C (Dipyridamole); DCR9Z582X0 (Epoprostenol); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
[Em] Mês de entrada:9403
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:940120
[St] Status:MEDLINE


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Fotocópia
[PMID]:8287616
[Au] Autor:Schirner M; Lichtner RB; Schneider MR
[Ad] Endereço:Research Laboratories of Schering AG, Berlin, Germany.
[Ti] Título:The stable prostacyclin analogue Cicaprost inhibits metastasis to lungs and lymph nodes in the 13762NF MTLn3 rat mammary carcinoma.
[So] Source:Clin Exp Metastasis;12(1):24-30, 1994 Jan.
[Is] ISSN:0262-0898
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Prostacyclin and its stable analogues have been shown to interfere specifically with certain steps of the metastatic cascade. The antimetastatic activity of the stable prostacyclin analogue Cicaprost (Schering AG) on haematogenous metastasis in a series of tumours in rats and mice has been well established. In order to test the effect of Cicaprost on lymphogenous metastasis we chose the metastatic cell clone MTLn3 derived from the 13762NF rat mammary carcinoma. The effect of Cicaprost on prevention of lung metastasis, lymph node metastasis and primary tumour growth was investigated. Cicaprost given in daily doses of 0.01, 0.03 and 0.1 mg/kg orally, reduced the number of lung metastases in a dose-dependent manner. Whereas the median number of lung metastases in the controls was greater than 1000, Cicaprost at a dose of 0.1 mg/kg reduced the number of lung metastases to between 11 and 100. The weight of the ipsilateral axillary lymph nodes was diminished by Cicaprost to 30-50% of controls. Moreover, metastasis to the contralateral axillary lymph node was completely inhibited by Cicaprost at all three doses tested. Cicaprost did not influence the growth rate of the MTLn3 cell clone implanted into the mammary fat pad or the weight of the primary tumour at the end of treatment. In conclusion, in addition to its dose-dependent effect on haematogenous metastasis, Cicaprost strongly inhibits lymph node metastasis.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Epoprostenol/análogos & derivados
Neoplasias Pulmonares/secundário
Metástase Linfática/prevenção & controle
Neoplasias Mamárias Experimentais/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Epoprostenol/uso terapêutico
Feminino
Neoplasias Pulmonares/prevenção & controle
Neoplasias Mamárias Experimentais/patologia
Mopidamol/uso terapêutico
Ratos
Ratos Endogâmicos F344
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 4Q0IWP8B8O (Mopidamol); DCR9Z582X0 (Epoprostenol); NE94J8CAMD (cicaprost)
[Em] Mês de entrada:9402
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:940101
[St] Status:MEDLINE


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Fotocópia
[PMID]:7870694
[Au] Autor:de la Cruz JP; Moreno A; Mérida F; García-Campos J; Sánchez de la Cuesta F
[Ad] Endereço:Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain.
[Ti] Título:The pyrimido-pyrimidine derivatives, dipyridamole and RA-642, reduce opacification of crystalline lens in diabetic rats.
[So] Source:Pharmacol Toxicol;75(5):250-4, 1994 Nov.
[Is] ISSN:0901-9928
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:We assessed the effect of dipyridamole, RA-642 and mopidamol, on lenticular opacities in a model of experimental diabetic cataracts in rats. All three pyrimido-pyrimidine derivatives caused a statistically significant reduction of opacification in crystalline lens as compared with untreated diabetic animals. The production of superoxide anions (phenazine methosulphate [PMS]-induced nitroblue tetrazolium [NBT] reduction) showed a decrease of 81.6%, 78.9% and 1.8% in lens tissue homogenates from rats treated with dipyridamole, RA-642 and mopidamol, respectively. Dipyridamole and RA-642 produced a statistically significant inhibition (50% and 64.8%, respectively) of lipid peroxidation (ferrous sulphate and ascorbic acid [FeAs]-induced malondialdehyde [MDA] production) as compared with the group of untreated diabetic rats. Mopidamol did not exert any inhibitory effect on lipid peroxidation. There was a statistically significant correlation between opacification of lens and PMS-induced NBT reduction and FeAs-induced MDA production. We conclude that the protective effect of dipyridamole and RA-642 from free radical damage to crystalline lens in the model of experimental diabetes used in this study, is the result of the antioxidant action of these compounds. The effect exerted by mopidamol, however, suggest a possible complementary effect of the pyrimido-pyrimidine derivatives through interaction with other mechanisms (e.g., the sorbitol pathway) implicated in the development of cataracts.
[Mh] Termos MeSH primário: Cardiotônicos/farmacologia
Catarata/prevenção & controle
Diabetes Mellitus Experimental/complicações
Dipiridamol/farmacologia
Cristalino/efeitos dos fármacos
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Glicemia/análise
Catarata/etiologia
Catarata/patologia
Cristalino/metabolismo
Cristalino/patologia
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Malondialdeído/metabolismo
Mopidamol/farmacologia
Ratos
Ratos Wistar
Superóxidos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Cardiotonic Agents); 0 (Pyrimidines); 11062-77-4 (Superoxides); 4Q0IWP8B8O (Mopidamol); 4Y8F71G49Q (Malondialdehyde); 54093-30-0 (RA 642); 64ALC7F90C (Dipyridamole)
[Em] Mês de entrada:9503
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:941101
[St] Status:MEDLINE


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Fotocópia
[PMID]:8453569
[Au] Autor:Tzanakakis GN; Agarwal KC; Vezeridis MP
[Ad] Endereço:Surgical Service Veterans Administration Medical Center, Providence, Rhode Island.
[Ti] Título:Prevention of human pancreatic cancer cell-induced hepatic metastasis in nude mice by dipyridamole and its analog RA-233.
[So] Source:Cancer;71(8):2466-71, 1993 Apr 15.
[Is] ISSN:0008-543X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Several studies have provided evidence suggesting that platelets play a key role in tumor metastasis. A number of antiplatelet agents have been used to prevent tumor metastasis in animal models and humans. Antiplatelet agents, dipyridamole (adenosine transport inhibitor), and RA-233 (inhibitor of cAMP PDE) were used to prevent tumor-cell-platelet interactions both in in vitro and in vivo systems; however, the data were not very conclusive. METHODS: Our studies used dipyridamole and RA-233 alone and in combination to investigate their effects on human pancreatic tumor cells (RWP-2)-induced platelet aggregation in human blood and on hepatic metastasis in nude mice. To examine effects of dipyridamole and RA-233 on liver metastasis, the tumor cells (RWP-2) were injected intrasplenically in nude mice grouped into control, dipyridamole (8 mg/kg), RA-233 (8 mg/kg), and dipyridamole plus RA-233 (8 mg/kg each). The agents were administered intraperitoneally 1 hour before and 24 hours after the tumor cell injection. RESULTS: When dipyridamole and RA-233 were used alone, only weak to moderate effects were seen on RWP-2 tumor cell-induced platelet aggregation. However, these agents, when combined, strongly inhibited the tumor cell-induced aggregation in human platelet-rich plasma. In tumor metastasis experiments, reductions of approximately 70% in hepatic nodules and 90% in surface area occupied by the tumor were seen with the combination treatment (dipyridamole plus RA-233) as compared with the control group of mice. CONCLUSIONS: This study suggests that the combination of dipyridamole and RA-233 provides an effective intervention for the antithrombotic approach to the treatment of cancer metastases.
[Mh] Termos MeSH primário: Dipiridamol/farmacologia
Neoplasias Hepáticas/prevenção & controle
Neoplasias Hepáticas/secundário
Mopidamol/farmacologia
Neoplasias Pancreáticas
Agregação Plaquetária/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenosina/sangue
Animais
Ensaios de Seleção de Medicamentos Antitumorais
Sinergismo Farmacológico
Seres Humanos
Neoplasias Hepáticas/sangue
Camundongos
Camundongos Nus
Neoplasias Pancreáticas/sangue
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
4Q0IWP8B8O (Mopidamol); 64ALC7F90C (Dipyridamole); K72T3FS567 (Adenosine)
[Em] Mês de entrada:9304
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:930415
[St] Status:MEDLINE


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Fotocópia
[PMID]:1522764
[Au] Autor:de la Cruz JP; Carrasco T; Ortega G; Sanchez de la Cuesta F
[Ad] Endereço:Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain.
[Ti] Título:Inhibition of ferrous-induced lipid peroxidation by pyrimido-pyrimidine derivatives in human liver membranes.
[So] Source:Lipids;27(3):192-4, 1992 Mar.
[Is] ISSN:0024-4201
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The effects of pyrimido-pyrimidine derivatives (dipyridamole, RA-642, and RA-233) on lipid peroxidation, using d-alpha-tocopherol as standard, were studied in enriched membrane fractions from human and rat hepatocytes. Equimolar concentrations of ferrous sulfate and ascorbic acid were used to induce lipid peroxidation. The amount of peroxidized lipids observed in membrane fractions from human liver was smaller than in those from rat liver. In both species, however, pyrimido-pyrimidine derivatives, except for RA-233 in rat liver, inhibited lipid peroxidation dose-dependently in the following sequence: RA-642 greater than dipyridamole greater than d-alpha-tocopherol RA-233.
[Mh] Termos MeSH primário: Membrana Celular/metabolismo
Compostos Ferrosos/farmacologia
Peroxidação de Lipídeos/efeitos dos fármacos
Fígado/metabolismo
Mopidamol/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Ácido Ascórbico/farmacologia
Cardiotônicos/farmacologia
Membrana Celular/efeitos dos fármacos
Dipiridamol/farmacologia
Seres Humanos
Cinética
Malondialdeído/metabolismo
Ratos
Especificidade da Espécie
Vitamina E/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Ferrous Compounds); 0 (Pyrimidines); 1406-18-4 (Vitamin E); 39R4TAN1VT (ferrous sulfate); 4Q0IWP8B8O (Mopidamol); 4Y8F71G49Q (Malondialdehyde); 54093-30-0 (RA 642); 64ALC7F90C (Dipyridamole); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:9210
[Cu] Atualização por classe:170905
[Lr] Data última revisão:
170905
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:920301
[St] Status:MEDLINE



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