Letteratura scientifica selezionata sul tema "Omeprazole"
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Articoli di riviste sul tema "Omeprazole"
Sartika, Eria, Eko Suhartono e Agung Biworo. "PENGARUH LANSOPRAZOL DAN OMEPRAZOL TERHADAP AKTIVITAS ENZIM KATALASE HEPAR TIKUS". Berkala Kedokteran 12, n. 2 (7 ottobre 2016): 255. http://dx.doi.org/10.20527/jbk.v12i2.1875.
Testo completoFienda, Adrully El, e Ainun Wulandari. "Analisis Efektivitas Biaya Penggunaan Omeprazol dan Pantoprazol dalam Terapi Peptic Ulcer pada Pasien Lansia Rawat Inap di Rumah Sakit Umum Adhyaksa". Jurnal Farmasi Higea 14, n. 2 (30 dicembre 2022): 169. http://dx.doi.org/10.52689/higea.v14i2.475.
Testo completoHutahaean, Amsaline, Gayatri Citraningtyas e Defny S. Wewengkang. "ANALISIS EFEKTIVITAS BIAYA PADA PASIEN GASTRITIS RAWAT INAP DI RUMAH SAKIT BHAYANGKARA MANADO". PHARMACON 8, n. 4 (28 novembre 2019): 767. http://dx.doi.org/10.35799/pha.8.2019.29351.
Testo completoNasrullah, Mohammed Z., Khalid Eljaaly, Thikryat Neamatallah, Usama A. Fahmy, Abdulmohsin J. Alamoudi, Hussain T. Bakhsh e Ashraf B. Abdel-Naim. "Omeprazole Prevents Colistin-Induced Nephrotoxicity in Rats: Emphasis on Oxidative Stress, Inflammation, Apoptosis and Colistin Accumulation in Kidneys". Pharmaceuticals 15, n. 7 (23 giugno 2022): 782. http://dx.doi.org/10.3390/ph15070782.
Testo completo&NA;. "Omeprazole see Furosemide/omeprazole". Reactions Weekly &NA;, n. 354 (giugno 1991): 11. http://dx.doi.org/10.2165/00128415-199103540-00049.
Testo completoJaved, Mamoona, Muhammad Hayder Ali, Muhammad Saad Tanveer e Muhammad Hassan Tanveer. "Omeprazole vs Lansoprazole in the Management of Gastroesophageal Reflux Disease: A Systematic Literature Review". Journal of Medical Research and Innovation 4, n. 2 (29 marzo 2020): e000204. http://dx.doi.org/10.32892/jmri.204.
Testo completoSkvortsova, T. A., G. Yu Knorring e E. N. Kareva. "Use of Omeprazole in Paediatric Patients in Russia". Doctor.Ru 20, n. 10 (2021): 39–43. http://dx.doi.org/10.31550/1727-2378-2021-20-10-39-43.
Testo completo&NA;. "Omeprazole". Reactions Weekly &NA;, n. 1382 (dicembre 2011): 28. http://dx.doi.org/10.2165/00128415-201113820-00100.
Testo completo&NA;. "Omeprazole". Reactions Weekly &NA;, n. 1386 (gennaio 2012): 29–30. http://dx.doi.org/10.2165/00128415-201213860-00102.
Testo completo&NA;. "Omeprazole". Reactions Weekly &NA;, n. 1390 (febbraio 2012): 28. http://dx.doi.org/10.2165/00128415-201213900-00108.
Testo completoTesi sul tema "Omeprazole"
Marostica, Marta Contieri. "Efeito do tratamento com inibidores de secreção acida na infecção por Helicobacter Pylori em camundongos". [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311373.
Testo completoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: O mecanismo pelo qual o H. pylori provoca a inflamação gástrica inclui a secreção de substâncias pró-inflamatórias pela bactéria e a estimulação da liberação de citocinas induzida pelo contato direto entre a bactéria e as células epiteliais gástricas. A resposta inicial à infecção por H. pylori é predominantemente neutrofílica e estes, liberam mediadores inflamatórios e enzimas proteolíticas que induzem o dano gástrico. Estresse oxidativo ocorre em pacientes infectados com H. pylori onde a expressão de enzimas como a óxido nítrico sintase induzida (iNOS), superóxido dismutase e catalase encontram-se aumentadas. A iNOS participa da resposta inflamatória e promove a apoptose de células na mucosa gástrica. Durante a infecção por H. pylori, observa-se níveis reduzidos da expressão de Bcl-2 e o aumento da expressão de Bax na mucosa gástrica, sugerindo que uma tendência pró-apoptótica na infecção. A erradicação pode ser alcançada pela combinação de antibióticos associada a uma droga anti-ácida. As duas maiores classes de inibidores de secreção ácida são: os inibidores de bomba protônica, como o omeprazol, e os antagonistas de receptor de histamina H2, como a ranitidina. Várias evidências experimentais têm mostrado que o omeprazol apresenta efeitos anti-ulcerogênicos adicionais. Deste modo, o objetivo deste trabalho foi avaliar o efeito do tratamento com omeprazol e ranitidina em um modelo animal de infecção por H. pylori, enfocando possíveis propriedades adicionais destes fármacos Para este estudo foram utilizados camundongos machos C57BL/6 com 4 semanas de idade. Os camundongos receberam por via oro-gástrica suspensão de H. pylori. Na 11ª semana de inóculo, os animais foram tratados (i.p.) com omeprazol (100 mg/kg), ranitidina (100 mg/kg) ou veículo (PBS) durante 7 dias sempre no mesmo horário. As duas drogas inibiram a produção de ácido gástrico no tratamento agudo, porém no tratamento por uma semana, apenas o omeprazol inibiu a secreção ácida. Os animais tratados com omeprazol apresentaram um aumento significativo nos níveis de colonização gástrica e elevado nível de MPO. Ambas as drogas diminuíram as lesões da mucosa provocada pela infecção. O tratamento com omeprazol restaurou a produção de Bcl-2 na mucosa gástrica e não alterou a produção de Bax. O omeprazol não protegeu a mucosa gástrica contra o dano ao DNA gerado pela infecção e o tratamento com ranitidina aumentou os níveis de dano oxidativo ao DNA. Não observamos a presença de propriedades anti-neutrofílicas, atribuídas ao omeprazol, após uma semana de tratamento, sugerindo que essas propriedades são restrita a ensaios in vitro. Entretanto, o omeprazol restaurou a produção de Bcl-2 na mucosa gástrica, sugerindo uma atividade anti-apoptótica dessa droga
Abstract: H. pylori induces gastric inflammation characterized by secretion of pro-inflammatory substances by bacteria and the stimulation of cytokine release by the gastric epithelial cells. The initial response to the H. pylori infection is predominantly by neutrophils and these cells liberate inflammatory mediators and enzymes that induce the gastric damage. Oxidative stress also occurs in infected patients where induced nitric oxide sintase (iNOS), superoxide dismutase and catalase expression were increased. Nitric oxide participates in the inflammatory response and promotes apoptosis of gastric mucosa cells. Eradication therapy can be achieved with antibacterial agents in association with anti-acid drugs. There are two major classes of gastric acid inhibitors: the proton pump inhibitors, such as omeprazole, and the histamine H2 receptor antagonists, such as ranitidine. Some experimental evidence demonstrates that omeprazole has additional pharmacological properties. Thus, the aim of this study was to evaluate the effect of omeprazole and ranitidine treatment on H. pylori-infected mice, focusing on possible additional pharmacological properties. For this study, male C57BL/6 mice that received H. pylori suspension were used. After the 11th week, the mice were treated intraperitoneally (i.p.) with omeprazole (100 mg/kg), ranitidine (100 mg/kg) or vehicle (PBS) for 7 days. Both drugs inhibited the gastric acid production after acute administration; however after one week of treatment just omeprazole inhibited gastric acid secretion. Omeprazole-treated mice presented an increase in H. pylori and MPO levels in gastric mucosa. Both drugs reduced the mucosa damage provoked by H. pylori infection. Omeprazole treatment restored the Bcl-2 production in the gastric mucosa and did not modify Bax production. Omeprazole did not reduce the DNA damage in the gastric mucosa while ranitidine treatment increased it. We conclude that some additional omeprazole-related properties, such as antineutrophil properties, were not observed in H. pylori-infected mice after one week of treatment. However, the antiapoptotic activity of omeprazole could be attributed to an ability to modify the protein expression of Bcl-2, decreased by H. pylori infection
Mestrado
Patologia Clinica
Mestre em Ciências Médicas
Freitas, Alessandra Ferraiolo de. "Caracterização e aplicação da fase estacionaria quiral tris(3,5-dimetilfenilcarbamato) de amilose na separação preparativa dos enantiomeros do omeprazol". [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/267135.
Testo completoTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Engenharia Quimica
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Resumo: O objetivo deste trabalho foi a síntese, em larga escala, da fase estacionária quiral tris(3,5-dimetilfenilcarbamato) de amilose e posterior investigação desta na separação preparativa dos enantiômeros do omeprazol por cromatografia líquida de alta eficiência. O carbamato de amilose, caracterizado por análise elementar e espectroscopia na região do infravermelho, apresentou valores experimentais de CHN próximos aos valores teóricos e absorções no infravermelho próximas a 1720 cm-1, referente ao grupo C=O, a 1220 cm-1, referente à ligação C-N e em 3294 cm-1, referente à ligação N-H. Experimentos de pulsos com soluções do traçador e da mistura racêmica, em diferentes temperaturas e vazões da fase móvel, foram realizados para avaliar a homogeneidade das colunas e sua influência no processo de separação, os coeficientes de dispersão axial e de tranferência de massa e o comportamento termodinâmico da adsorção. Uma análise estatística dos dados de porosidade foi realizada através dos testes t e F mostrando que, com um nível de confiança de 95%, apenas algumas colunas apresentam porosidades equivalentes embora os erros cometidos na determinação da porosidade total e no processo de empacotamento sejam os mesmos. A recuperação do enantiômero de interesse, S-(-)-omeprazol, variou de 10-100% quando a porosidade total sofreu variações da ordem de 3%. Os gráficos de van Deemter mostraram uma relação linear entre a altura equivalente a um prato e a velocidade superficial da fase móvel. O enantiômero S-(-)- apresentou maiores coeficientes de transferência de massa e o enantiômero R-(+)- maiores constantes de Henry. O fator de separação e a resolução apresentaram valores iguais a 1,30 e 1,96, respectivamente, a 40 °C e 1,0 mL/min. Observou-se um decréscimo nos valores desses parâmetros após um determinado tempo de uso da coluna. Os valores negativos de 0 S D e 0 H D indicam um aumento na ordem do sistema cromatográfico e que a adsorção dos enantiômeros da fase móvel na fase estacionária é entalpicamente favorável. O modelo de isoterma de Langmuir foi bem correlacionado aos dados experimentais de equilíbrio no intervalo de concentração analisado. Palavras-chave: fase estacionária quiral, omeprazol, cromatografia líquida de alta eficiência
Abstract: The aim of this work was the synthesis, in large scale, of the amylose tris(3,5- dimethylphenylcarbamate) chiral stationary phase and further evaluate in the omeprazole enantiomer preparative separation by high performance liquid chromatography. The amylose carbamate, characterized by elemental analysis and infrared spectroscopy, showed CHN experimental values close to theoretical values and infrared absorptions at 1720 cm-1 which is assigned to C=O group, at 1220 cm-1 which is assigned to C-N bond and at 3294 cm-1 which is assigned to N-H bond. Pulse experiments with solutions of the inert and racemic mixture at different flow rates and temperature were carried out to evaluate column homogeneity and its influence on separation process, axial dispersion and mass transfer coefficients and adsorption thermodynamic behavior. A statistical analysis of the porosity data was performed through of the t and F tests showing that with 95% confidence level only some columns presented equivalent porosities although the errors made in the total porosity determination and packing process are equal. The recovery of the interest enantiomer, S-(-)-omeprazole, varied of 10 until 100% when total porosity varied in the order of 3%. The van Deemter plots showed a linear dependence between height equivalent to a theoretical plate and mobile phase superficial velocity. S-(-)- enantiomer presented higher values of mass transfer coefficients and the enantiomer R-(+)-omeprazole presented higher values of Henry constants. The separation factor and resolution values were 1.30 and 1.96 at 40 °C and 1.0 mL/min, respectively. It was observed a decrease of these parameter values after a use time of the column. The negative values of 0 S D and 0 H D indicates an increase in the order of chromatographic system and that the enantiomer adsorption from the mobile phase to stationary phase is enthalpically favorable. The Langmuir isotherm model was well correlated to equilibrium experimental data in the range of investigated concentration. Key-words: chiral stationary phase, omeprazole, high performance liquid chromatography
Doutorado
Desenvolvimento de Processos Biotecnologicos
Doutor em Engenharia Química
Rocha, Adriana. "Enantiosseletividade no metabolismo do citalopram associado a inibidores do CYP: estudos clínicos e experimental". Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/60/60134/tde-29072009-142313/.
Testo completoCitalopram (CITA), a selective serotonin reuptake inhibitor, is available for clinical use as a racemic mixture of the (+)-(S) and (-)-(R) enantiomers or as the pure (+)-(S)-CITA enantiomer. CITA is metabolized by CYP2C19, CYP2D6 and CYP3A to demethylcitalopram (DCITA) and by CYP2D6 to didemethylcitalopram. The present study investigated the influence of enzyme inhibitors on the enantioselective metabolism of CITA in rats and healthy volunteers. Male Wistar rats (n=6 for each group) received a single dose of 20 mg/kg CITA (control group) or were pretreated with 80 mg/kg quinidine (quinidine group), 10 mg/kg fluvoxamine (fluvoxamine group), or 50 mg/kg ketoconazole (ketoconazole group). Blood samples were collected from the animals up to 20 h after the administration of CITA. Healthy volunteers phenotyped as extensive metabolizers of CYP2C19 (omeprazole as marker drug) and of CYP2D6 (debrisoquine as marker drug) and those with normal CYP3A activity (midazolam as marker drug) received a single oral dose of 20 mg racemic CITA combined or not with omeprazole (20 mg/day for 18 days). The CITA and DCITA enantiomers were analyzed by LC-MS/MS using a Chiralcel OD-R chiral column and a mobile phase of acetonitrile:methanol:water (30:30:40, v/v/v) containing 0.05% diethylamine. The method was linear in the concentration range of 0.1-20 ng of each CITA and DCITA enantiomer/mL human plasma and of 0.1-500 ng of each CITA and DCITA enantiomer/mL rat plasma. Accuracy and precision were below the acceptance limits of 15% for human and rat plasma. The kinetic disposition of CITA was enantioselective in rats of the control (AUCS/R ratio = 0.4), quinidine (AUCS/R ratio = 0.5) and ketoconazole (AUCS/R ratio = 0.8) groups. The inhibition of CYP2D by quinidine resulted in the non-enantioselective inhibition of the metabolism of CITA and DCITA. The inhibition of CYP2C by fluvoxamine and of CYP3A by ketoconazole only inhibited the metabolism of (+)-(S)-CITA. The kinetic disposition of CITA in healthy volunteers was enantioselective in the absence of treatment with omeprazole, with the observation of a higher plasma proportion of the (-)-(R)-CITA enantiomer. The AUCS/R ratio was 0.56 for CITA and 1.06 for the DCITA metabolite. The administration of racemic CITA to healthy volunteers treated with omeprazole showed a loss of enantioselectivity in the pharmacokinetics of CITA. The AUCS/R ratio was 0.96 for CITA and 0.92 for DCITA. The administration of multiple doses of omeprazole to healthy volunteers enantioselectively inhibited the metabolism of the (+)-(S)-CITA eutomer, with an approximately 140% increase of plasma concentrations
Lopes, Jéssica Maria Sanches. "Efeitos de drogas inibidoras da secreção ácida do estômago sobre as respostas hipotensoras do nitrito de sódio". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-17042018-161320/.
Testo completoNitrite can be reduced to NO depending on acidic pH of the stomach or by enzymes with nitrite reductase activity. Treatment with omeprazole attenuates the antihypertensive effects of oral nitrite by increasing of gastric pH. However, studies are still necessary to further evaluate wheter ranitidine is also able to attenuate the antihypertensive effects of sodium nitrite by increasing gastric pH. In this study, we examined whether oral administration of ranitidine could impair oral antihypertensive effects of sodium nitrite by interfering with the formation of NO and nitrosylated species from nitrite. In order to analyze the influence of ranitidine under hypotensive effect of sodium nitrite, rats were treated with L-NAME and pretreated with ranitidine, omeprazole, vehicle or buffer, subsequently all the groups were treated with sodium nitrite 15 mg/kg. The L-NAME treatment increase mean arterial pressure (MAP). The gastric pH was different among the groups, there was an increased in rats gastric pH treated with ranitidine and omeprazole compared to the vehicle. The buffer group had the same pH of vehicle and drugs treatment. Sodium nitrite exerted significant antihypertensive effects in the groups studied. However, lesser decreases in MAP were observed in rats treated with omeprazole and ranitidine compared to rats that received vehicle. These findings were associated with a lower NO gastric concentrations as well as nitrosylated species plasma levels. In addition, there was an increased in nitrite concentrations in the stomach. No differences were observed in plasma nitrite levels. Moreover, there was not any significant difference in plasma and stomach NOx levels among the studied groups. The rats treated with buffer showed similar results to those treated with the drugs. Together these data demonstrated that ranitidine, through increased gastric pH, affects antihypertensive responses to oral sodium nitrite by reducing the formation of NO and nitrosylated species. This fact is reinforced by higher levels in nitrite concentrations in the stomach, thereby it suggests a lower conversion of nitrite to NO and nitrosylated species in the gastric environment.
Jackson, Remonica, Stacy D. Brown e Paul Lewis. "Comparative Stability of Compounded Omeprazole Suspension Versus Commercial Omeprazole Kit When Stored in Oral Syringes Under Refrigerated Conditions". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/7847.
Testo completoGwerder, Christoph. "Individually feedback-titrated 48h infusions of omeprazole /". [S.l : s.n.], 1994. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
Testo completoPinheiro, Lucas Cézar. "Estudo de mecanismos anti-hipertensivos do nitrito de sódio na hipertensão renovascular experimental". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-18032015-230532/.
Testo completoNitric Oxide plays many functional roles in physiological systems. In the cardiovascular system it participates in a unique way in the regulation of vascular tone among other functions. Dysfunctions in the production or availability of NO may compromise their physiological activity and participate in hypertension. Besides the production of NO by the nitric oxide synthase, other physiological pathways of NO production from nitrite have been described. The nitrite and nitrate are oxidation products of NO. Further nitrite is oxidized to nitrate. These three molecules are known to forma cycle in the body. Nitrate is excreted in saliva and reduced to nitrite by oral bacteria. Nitrite then is swallowed with the saliva and exerts its effects through conversion to NO. The conversion of nitrite to NO may occur by enzymatic or non-enzymatic manner. As a non-enzymatic way nitrite is reduced to NO by reaction with H+.This reaction occurs mainly in the stomach. This thesis aims to elucidate possible mechanisms responsible for the antihypertensive effects of sodium nitrite. We studied 2K1C rats treated with nitrite and nitrate and checked anti-hypertensive effects of these molecules. The increased gastric pH by omeprazole prevented the anti-hypertensive effect of nitrite and nitrate. Omeprazole did not cause any differences in plasma nitrite and nitrate. It was found that treatment with nitrite and nitrate resulted inincreased nitrosylated species in the plasma, and this increase was blocked by omeprazole. We also tested the influence of the entero-salivarycycle effect of nitrite and nitrate. We found that treatment with mouthwash blunted the antihypertensive effect of nitrate but this effect did not change in animals treated with nitrite. Interestingly in all experimental approaches the anti-hypertensive effect of nitrite only occurred when there was an increase in the plasma concentration of nitrosylated species
Peloso, Leonardo José. "A concentração sérica de tacrolimo após a ingestão de omeprazol: um estudo piloto". Universidade Federal de Uberlândia, 2014. https://repositorio.ufu.br/handle/123456789/12810.
Testo completoIntrodução: Tacrolimo (TCR) é uma droga imunossupressora amplamente utilizada em receptores de órgãos pós-transplantes. Sua absorção ocorre principalmente no duodeno e jejuno, sua concentração sérica máxima é atingida entre 0,5 e 4 horas após a ingestão (média de 2 horas) e sua absorção pode ser facilitada em meio alcalino. Omeprazol (OMP) é um inibidor da bomba de protóns das células parietais do estômago e atinge sua concentração máxima entre 0,5 e 3,5 horas após a ingestão (média de 2 horas) e uma vez que reduz a acidez gástrica, é capaz de libertar o conteúdo mais alcalino para o duodeno. Interações farmacológicas entre TCR e OMP são descritas principalmente com relação à via metabólica comum (CYP3A4 e P-gp) utilizadas por ambos medicamentos, que pode resultar em elevações da concentração plasmática do TCR. Os objetivos deste trabalho são: identificar se há aumento ou diminuição da concentração de tacrolimo quando administrado após o omeprazol e determinar a frequência de sujeitos que aumentaram, em 2 horas, a biodisponibilidade de tacrolimo após o uso do omeprazol. Sujeitos e Métodos: Foi realizado um estudo piloto, duplo cego, cruzado contra placebo em 28 sujeitos pós transplante renal em uso regular de TCR (média: 0,08 ± 0,05 mg/kg de peso/dia BID) e OMP (20 mg/dia MID). Diariamente o OMP ou placebo foram ingeridos em jejum pela manhã às 6:00 horas e, após 2 horas, o TCR foi ingerido nas doses relatadas anteriormente. As coletas de sangue foram realizadas 2 horas após a ingestão do TCR ao final de 4 dias consecutivos, tanto em regime de OMP quanto placebo, sendo o sujeito o controle dele mesmo. As concentrações séricas do TCR foram obtidas pelo método de imunoensaio quimioluminescente por micropartículas em sangue total humano (CMIA, Abbott Lab. do Brasil) em jejum alimentar de 3,5 horas. Resultados: Dos sujeitos avaliados: 18 (64,3%) eram do sexo masculino e 10 (35,7%) feminino; 8 (28,6%) obtiveram rim de doador vivo e 20 (71,4%) de doador cadáver. A idade média dos sujeitos foi 43 ± 13 anos e o tempo pós transplante de 41 ± 32 meses. As dosagens médias de creatinina e ureia séricas foram de 1,6 ± 0,5 mg/dL e 59 ± 27 mg/dL, respectivamente, e hemoglobina de 13,7 ± 1,9 g%. Quanto às médias das concentrações séricas de TCR obtidas em uso de placebo ou OMP não mostraram diferenças significativas (15,8 ± 8,7 ng/mL versus 15,7 ± 6,8 ng/mL; respectivamente; P=0,92). Conclusão: Em nosso estudo foi possível observar que a ingestão do OMP, previamente ao TCR, não alterou as concentrações séricas médias do referido imunossupressor; entretanto, em relação ao período placebo houve aumento na concentração sérica do TCR acima de 10% em 13 sujeitos e acima de 20% em 10 sujeitos, o que correspondeu a 46,4% e 35,7%, respectivamente, dos sujeitos de pesquisa. Estes dados inferem que o OMP, se ingerido 2 horas antes do TCR, pode aumentar a concentração sérica deste imunossupressor por provável alcalinização do conteúdo intestinal. Estes dados serão utilizados nos cálculos de tamanho amostral, para futuros estudos com maior número de sujeitos.
Mestre em Ciências da Saúde
Pinheiro, Lucas Cézar 1986. "Omeprazol atenua os efeitos anti-hipertensivos do nitrito de sódio em ratos". [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310022.
Testo completoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: O óxido nítrico (NO) regula diversos sistemas orgânicos. Disfunções na produção ou disponibilidade de NO podem comprometer sua atuação fisiológica. Além da produção de NO pelas óxido nítrico sintetases, outras vias de produção de NO são relatadas, entre elas a conversão de nitrito a NO. O nitrito é o produto inicial da oxidação do NO, sendo posteriormente oxidado a nitrato. Sabe-se que estas três moléculas formam um ciclo dentro do organismo. A conversão de nitrito a NO pode ocorrer de forma enzimática ou não enzimática. Como forma não enzimática, o nitrito é convertido a NO pela reação com H+. Esta reação ocorre principalmente no estômago, todavia não se sabe se este NO formado tem efeito na pressão arterial sistêmica ou atua apenas localmente. A fim de verificar a influência do pH gástrico no efeito hipotensor do nitrito de sódio, utilizamos animais tratados agudamente com LNAME e normotensos canulados acordados pré-tratados com omeprazol e, posteriormente, com nitrito de sódio 15mg/kg e 45mg/kg. Foi verificado que o nitrito de sódio reduz a pressão arterial média dos animais significativamente e de maneira dependente da dose. O pré-tratamento com omeprazol reduziu o efeito hipotensor do nitrito de sódio significativamente. Após, foram quantificados os níveis de nitrito e nitrato. Foi observado aumento em ambos após o tratamento com nitrito de sódio. A partir destes resultados podemos sugerir que o omeprazol atenua o efeito hipotensor do nitrito de sódio em ratos normotensos e hipertensos
Abstract: Many body systems are regulated by nitric oxide (NO). Dysfunctions in the production or availability of NO may impair it physiological roles. However, other routes of NO production are reported in addition to NO production by nitric oxide synthases, including the conversion of nitrite to NO. Nitrite is the initial product of oxidation of NO and is further oxidized to nitrate. It is known that these three molecules form a cycle within the body. The conversion of nitrite to NO can occur enzymatic or nonenzymatic. Non-enzymatic nitrite is converted to NO by reacting with H+. This reaction occurs mainly in the stomach, however it is unclear whether this NO affects blood pressure or simply acts locally. To study the influence of gastric pH on the hypotensive effect of sodium nitrite, we used hypertensive or normotensive cannulated animals pretreated with omeprazole and with sodium nitrite 15 mg/kg and 45 mg/kg. We found that sodium nitrite reduces mean arterial pressure of animals in a dose-dependent manner. Pretreatment with omeprazole reduced the hypotensive effect of sodium nitrite significantly. Thereafter, we quantified the levels of nitrite and nitrate. We found increase in both species after treatment with sodium nitrite. These results suggest that omeprazole attenuates the hypotensive effect of sodium nitrite in normotensive and hypertensive rats
Mestrado
Farmacologia
Mestre em Farmacologia
Morgado, Aline Alberti. "Ação preventiva de fármacos antiácidos e potenciais biomarcadores para úlcera abomasal decorrente do uso de fenilbutazona em ovinos adultos". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-18062018-162112/.
Testo completoAbomasal ulcers reduce welfare and production of milk and meat, but information about their etiopathogenesis, diagnosis, prevention and treatment is still insufficient, especially for adult ruminants. Protocols used for prevention and treatment of this disease are extrapolated from those determined for gastric lesions in monogastric animals. However, there are still uncertainties about the preventive effect of these drugs, the used doses and best route of administration to ruminants. The preventive action of ranitidine and omeprazole on the development of abomasal ulcers was tested. The antacid drugs were administered concomitantly to phenylbutazone over seven days (4.4 mg/kg twice a day, intravenously). Eight healthy sheep, cannulated in abomasum, were distributed in two 4x4 Latin squares and treated with 2 mg/kg of ranitidine every 12 hours; 0.4 mg/kg of omeprazole, administered intravenously once a day; 4 mg/kg of omeprazole paste, administered orally once a day; or no antacid drug (control). Intravenously administered omeprazole caused phlebitis and a higher number of animals had lesions in the abomasal mucosa. Omeprazole paste was not effective in the prevention of type 1a ulcer. Although there was no difference between groups, ranitidine showed the lowest number of animals with lesions diagnosed by histological examination; however, this H2 antagonist caused an increase in heart rate. Measurements of pH and acidity of abomasal contents, serum pepsinogen and lysozyme concentrations, as well as fecal occult blood screening were concluded not to be valid biomarkers for type 1a abomasal ulcers in adult sheep.
Libri sul tema "Omeprazole"
Zomorodi, Katayoun. The interaction between omeprazole and diazepam: Investigations performed in various drugmetabolising systems. Manchester: University of Manchester, 1994.
Cerca il testo completoGrant, Okil. Omeprazole. Independently Published, 2018.
Cerca il testo completoRamy, Jamil. Omeprazole. Independently Published, 2018.
Cerca il testo completolaid, Jory. Omeprazole. Independently Published, 2018.
Cerca il testo completoLees, Michelle Anne. Omeprazole usage evaluation. 1992.
Cerca il testo completoOmeprazole & Acid Inhibition: The Essential Issues - Journal: Digestion, Suppl. 1, 1990 (Omeprazole & Acid Inhibition). S. Karger AG (Switzerland), 1991.
Cerca il testo completoThe Logic of Omeprazole: Treatment by Design. CoMed Communications, 2000.
Cerca il testo completoKasiwong, Srirat. Pharmacokinetics of ampicillin, gentamicin, amikacin, and omeprazole in llamas. 1997.
Cerca il testo completoStanley, Peter C. Amazon Basic Care Omeprazole: Acid Reducer, Treats Frequent Heartburn. Lulu Press, Inc., 2022.
Cerca il testo completoMethot, Linda. A drug use evaluation of omeprazole in adult KGH inpatients. 1999.
Cerca il testo completoCapitoli di libri sul tema "Omeprazole"
de Groot, Anton C. "Omeprazole". In Monographs In Contact Allergy, 703–5. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003158004-355.
Testo completoAlarcón, Teresa, Isabel Sánchez Romero, Diego Domingo, Aurora Limia, Francisco De Diaz Rojas e Manuel López-Brea. "Comparative in Vitro Synergy Study of Omeprazole/Clarithromycin versus Omeprazole/Amoxicillin". In Campylobacters, Helicobacters, and Related Organisms, 371–74. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9558-5_67.
Testo completoLabenz, J., E. Gyenes, U. Peitz e G. Börsch. "Ciprofloxacin-Omeprazole Treatment for Eradication of Helicobacter pylori". In Helicobacter pylori and Gastroduodenal Pathology, 337–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77486-7_61.
Testo completoLabenz, J., E. Gyenes, G. H. Rühl e G. Börsch. "Amoxicillin—Omeprazole Treatment for Eradication of Helicobacter pylori". In Helicobacter pylori and Gastroduodenal Pathology, 342–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77486-7_62.
Testo completoDent, J., G. Vantrappen e J. P. Isal. "Can Omeprazole allow healing of certain ulcerated esophagitis?" In Benign Lesions of the Esophagus and Cancer, 289–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73055-9_80.
Testo completoFesten, H. P. M., H. A. R. E. Tuynman e S. G. M. Meuwissen. "Omeprazole: A review of its pharmacological and clinical properties". In Peptic Ulcer Disease: Basic and Clinical Aspects, 127–41. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5034-4_10.
Testo completoDunjić, B. S., J. Axelson, M. S. Dunjić, M. Hashmonai e S. Bengmark. "Effects of Ranitidine, Omeprazole and Vagotomy on Rat Gastric Mucosal Phospholipids". In Cell Injury and Protection in the Gastrointestinal Tract, 139–45. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5392-8_14.
Testo completoLamers, C. B. H. W. "Omeprazole in the prevention and therapy of gastroduodenal lesions on NSAID therapy". In Side-Effects of Anti-Inflammatory Drugs 3, 154–58. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2982-4_19.
Testo completoWallmark, Björn. "New Approaches to Inhibition of Gastric Acid Secretion: Development and Mechanism of Omeprazole". In Molecular and Cellular Mechanisms of H+ Transport, 95–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79301-1_11.
Testo completoOwman, C., M. Lindvall-Axelsson e B. Winbladh. "Omeprazole, an Inhibitor of H+-K+-ATPase, Markedly Reduces CSF Formation in the Rabbit". In Intracranial Pressure VII, 312–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73987-3_83.
Testo completoAtti di convegni sul tema "Omeprazole"
M.Hussein, Ali, Nadir Nanakali e Mohammed M.Hussein. "EFFECT OF HYPERICUM PERFORATUM ON GASTRIC ULCER IN RAT". In 4th International Conference on Biological & Health Sciences (CIC-BIOHS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/biohs2022/paper.742.
Testo completoSilva, Wilienne Gabriela Torres Da, Nathany França Pessoa e Rafaela Souza Silva. "PRESCRIÇÃO E USO DE OMEPRAZOL POR SONDA DE NUTRIÇÃO ENTERAL: REVISÃO SISTEMÁTICA". In III Congresso Brasileiro de Ciências Farmacêuticas On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbracif/38.
Testo completoSilitonga, Hendrika Andriana, Gontar Alamsyah Siregar, Rosita Juwita Sembiring e Marline Nainggolan. "Effect of Chayote (Sechium Edule Jacq. Swartz) Extract on Level of Interleukin-8 in Wistar Rats with Aspirin-Induced Gastritis". In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.35.
Testo completoHarrison, B., D. Despain, A. Mandagere, G. Walker e C. Dufton. "Omeprazole Has No Clinically Relevant Effect on the Pharmacokinetics of Ambrisentan." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3348.
Testo completoFatima, S., N. Sheikh e A. Tayyeb. "Investigation of hepatic and renal toxicity induced by omeprazole in CCl4 injury mouse model". In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677070.
Testo completoTangamornsuksan, Wimonchat, Pongpak Thiansupornpong, Thirawut Morasuk, Ornrat Lohitnavy e Manupat Lohitnavy. "A pharmacokinetic model of drug-drug interaction between clopidogrel and omeprazole at CYP2C19 in humans". In 2017 39th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2017. http://dx.doi.org/10.1109/embc.2017.8037415.
Testo completoCatapano, J., V. Fredrickson, A. Wakim, J. Lundberg, B. Hendricks, J. Baranoski, T. Cole et al. "E-216 The effect of omeprazole on patients taking clopidogrel after flow diverter device placement". In SNIS 17TH ANNUAL MEETING. BMA House, Tavistock Square, London, WC1H 9JR: BMJ Publishing Group Ltd., 2020. http://dx.doi.org/10.1136/neurintsurg-2020-snis.247.
Testo completoBHANOT, RAVINDER D. "Nosocomial Pneumonia In Mechanically Ventilated Patients Receiving Ranitidine, Omeprazole or Sucralfate As Stress Ulcer Prophylaxis". In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6039.
Testo completoConesa Nicolás, E., AM Chica Marchal, AC Viney, S. Nuñez Bracamonte, C. Juez Santamaría, A. Lloret Llorca, B. Fernández-Lobato, CN García Matillas e M. Martinez Penella. "3PC-046 Study of stability of two liquid formulations of omeprazole elaborated in the pharmaceutical service". In 24th EAHP Congress, 27th–29th March 2019, Barcelona, Spain. British Medical Journal Publishing Group, 2019. http://dx.doi.org/10.1136/ejhpharm-2019-eahpconf.127.
Testo completoPatlolla, Jagan Mohan R., Yuting Zhang, Li Qian, Vernon E. Steele e Chinthalapally V. Rao. "Abstract A141: Chemopreventive properties of omeprazole against azoxymethane‐induced colonic aberrant crypt foci formation in fats". In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Dec 6–9, 2009; Houston, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-09-a141.
Testo completoRapporti di organizzazioni sul tema "Omeprazole"
Xie, Cheng, Langhui Liu, Suyou Zhu e Mingquan Wei. Effectiveness and Safety of Chinese Medicine Combined with Omeprazole in the Treatment of Gastric Ulcer:A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, aprile 2021. http://dx.doi.org/10.37766/inplasy2021.4.0048.
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