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Статті в журналах з теми "Omeprazole"
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Sartika, Eria, Eko Suhartono, and Agung Biworo. "PENGARUH LANSOPRAZOL DAN OMEPRAZOL TERHADAP AKTIVITAS ENZIM KATALASE HEPAR TIKUS." Berkala Kedokteran 12, no. 2 (October 7, 2016): 255. http://dx.doi.org/10.20527/jbk.v12i2.1875.
Повний текст джерелаАнотація:
Abstract: Lansoprazole and omeprazole is a Proton Pump Inhibitor class of drugs that are often used for the treatment of peptic ulcers. Lansoprazole and omeprazole have an influence on the various target organs exposed. Mechanism of lansoprazole and omeprazole in influencing the activity of the enzyme catalase is competing with absolute catalase enzyme substrate (H2O2) in the binding of the enzyme active site. This study aims to determine the effect of lansoprazole and omeprazole against liver catalase enzyme activity. This study was a laboratory experimental study conducted in three groups, namely the control group (P0), the treatment group (P1) is given lansoprazole 30 mg and a treatment group (P2) given omeprazole 20 mg. The result showed the value of Km of the control group (P0) of 13.482 mmol/dm3, the treatment group (P1) of 11,227 mmol/dm3 and the treatment group (P2) of 6,327 mmol/dm3. Analysis of statistical data shows the regression correlation value of p for P1 was 0,01 adn for P2 was 0,02 (p <0.05) and the R value approaching 1 with a linear graph Lineweaver Burk meaningful. Concluded that lansoprazole and omeprazole may affect the activity of the liver enzyme catalase. Keywords: lansoprazole, omeprazole, enzyme catalase, rat liver Abstrak: Lansoprazol dan omeprazol merupakan obat golongan proton pump inhibitor yang sering digunakan untuk pengobatan tukak lambung. Lansoprazol dan omeprazol memiliki berbagai pengaruh terhadap organ target yang terpajan. Mekanisme lansoprazol dan omeprazol dalam mempengaruhi aktivitas enzim katalase adalah berkompetisi dengan substrat absolut enzim katalase (H2O2) dalam mengikat sisi aktif enzim. Penelitian ini bertujuan untuk mengetahui pengaruh lansoprazol dan omeprazol terhadap aktivitas enzim katalase hepar. Penelitian ini merupakan penelitian quasi eksperimental yang dilakukan pada 3 kelompok, yakni kelompok kontrol (P0), kelompok perlakuan (P1) diberikan lansoprazol 30 mg dan kelompok perlakuan (P2) diberikan omeprazol 20 mg. Hasil penelitian didapatkan nilai Km pada kelompok kontrol (P0) sebesar 13,482 mmol/dm3, pada kelompok perlakuan (P1) sebesar 11,227mmol/dm3 dan pada kelompok perlakuan (P2) sebesar 6,327mmol/dm3. Analisis data statistik korelasi regresi menunjukkan nilai p pada P1 0,01 dan pada P2 0,02 (p<0,05) serta nilai R mendekati 1 dengan grafik linear Lineweaver Burk yang menanjak. Disimpulkan bahwa lansoprazol dan omeprazol dapat mempengaruhi aktivitas enzim katalase hepar mencit. Kata-kata kunci: lansoprazol, omeprazol, enzim katalase, hepar mencit
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Fienda, Adrully El, and 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, no. 2 (December 30, 2022): 169. http://dx.doi.org/10.52689/higea.v14i2.475.
Повний текст джерелаАнотація:
PPI (proton pump inhibitors) adalah salah satu obat yang umum diresepkan pada gangguan lambung. Penelitian ini bertujuan untuk mengetahui nilai efektivitas biaya pada penggunaan Omeprazol dan Pantoprazol pada pasien rawat inap di RSU Adhyaksa. Penelitian ini menggunakan metode deskriptif kuantitatif dengan pengambilan data secara retrospektif dengan membandingkan Direct Medical Cost (biaya medik langsung). Subjek dari penelitian ini adalah semua pasien rawat inap di RSU Adhyaksa yang mendapatkan terapi Omeprazol dan Pantoprazol dengan usia >50 tahun dalam periode Januari 2020 – Mei 2022. Hasil efektivitas terapi dapat dilihat dari data rekam medis pasien dan biaya pengobatan pasien yang dianalisis dengan perhitungan rasio rerata efektivitas biaya (ACER). Berdasarkan efektivitas terapi pantoprazol (95,2%) lebih efektif dibandingkan omeprazol (90,5%). Terdapat perbedaan nilai ACER pada pasien yang menggunakan pantoprazole sebesar Rp 1.802.501,- dan pada omeprazole sebesar Rp 2.022.952,-. ICER pada penelitian ini menunjukkan angka Rp. 601.510,-. Pada penelitian ini terdapat perbedaan efektivitas antara pantoprazol dan omeprazole sebagai terapi Peptik ulser. Biaya terapi peptic ulser pada pantoprazol lebih rendah dibandingkan omeprazole.
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Hutahaean, Amsaline, Gayatri Citraningtyas, and Defny S. Wewengkang. "ANALISIS EFEKTIVITAS BIAYA PADA PASIEN GASTRITIS RAWAT INAP DI RUMAH SAKIT BHAYANGKARA MANADO." PHARMACON 8, no. 4 (November 28, 2019): 767. http://dx.doi.org/10.35799/pha.8.2019.29351.
Повний текст джерелаАнотація:
ABSTRACTGastritis is an inflammatory process in the gastric mucosa and submucosa or health problems caused by irritation and infection factors. Treatment therapy used in gastritis is the proton pump inhibitor (PPI), H2 receptor antagonists, and antacids. Giving treatment therapy used by patients has an impact on the amount of medical expenses. The purpose of this study was to determine a more cost effective therapy between the use of omeprazole and lansoprazole in hospitalized gastrtitis patients at Bhayangkara Hospital, Manado. The method used in this study is Cost Effectiveness Analysis with a retrospective data collection on the period of January - December 2018. The sample in this study was 44 patients, consisting of 25 patients using with omeprazole therapy and 19 patients with lansoprazole therapy. The results showed that the most cost-effective PPI was omeprazole with an ACER value of IDR 643,210.37 and ICER value of IDR 631,023.17/ day for each increase in effectiveness if there is a transfer from lansoprazole to omeprazole Keywords: Cost Effectiveness Analysis, Gastritis, Omeprazole, Lansoprazol. ABSTRAKGastritis adalah proses inflamasi pada mukosa dan submukosa lambung atau gangguan kesehatan yang disebabkan oleh faktor iritasi dan infeksi. Terapi pengobatan yang digunakan pada penyakit gastritis yaitu proton pump inhibitor (PPI), antagonis reseptor H2, serta antasida. Pemberian terapi pengobatan yang digunakan oleh pasien berdampak pada besarnya biaya pengobatan. Tujuan penelitian ini untuk menentukan terapi yang lebih cost effective antara penggunaan omeprazol dan lansoprazol pada pasien gastrtitis rawat inap di RS Bhayangkaara Manado. Metode yang digunakan pada penelitian ini adalah Cost-Effectiveness Analysis dengan rancangan pengambilan data secara retrospektif pada periode Januari – Desember 2018. Sampel pada penelitian ini sebanyak 44 pasien, terdiri dari 25 pasien pengguna terapi omeprazol dan 19 pasien pengguna terapi lansoprazol. Hasil penelitian menunjukkan terapi PPI yang lebih cost-effective adalah omeprazol dengan nilai ACER sebesar Rp. 643.210,37 dan nilai ICER sebesar Rp. 631.023,17/hari untuk setiap peningkatan efektivitas jika akan dilakukan perpindahan dari lansoprazol ke omeprazol. Kata Kunci : Analisis Efektivitas Biaya, Gastritis, Omeprazol, Lansoprazol.
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Nasrullah, Mohammed Z., Khalid Eljaaly, Thikryat Neamatallah, Usama A. Fahmy, Abdulmohsin J. Alamoudi, Hussain T. Bakhsh, and Ashraf B. Abdel-Naim. "Omeprazole Prevents Colistin-Induced Nephrotoxicity in Rats: Emphasis on Oxidative Stress, Inflammation, Apoptosis and Colistin Accumulation in Kidneys." Pharmaceuticals 15, no. 7 (June 23, 2022): 782. http://dx.doi.org/10.3390/ph15070782.
Повний текст джерелаАнотація:
The clinical value of colistin, a polymyxin antibiotic, is limited by its nephrotoxicity. Omeprazole is a commonly prescribed proton pump inhibitor. The current study aimed to evaluate the effects of the concomitant administration of omeprazole on colistin-induced nephrotoxicity in rats. Omeprazole significantly ameliorated colistin nephrotoxicity as evidenced by prevention in the rise in the serum level of creatinine, urea and cystactin C as well as urinary N-acetylglucosamine activity. This was confirmed by histological studies that indicated a decreased incidence of interstitial nephritis, degenerative cortical changes and collagen deposition. This was accompanied by the prevention of oxidative stress as omeprazole significantly inhibited the lipid peroxidation, glutathione depletion and enzymatic exhaustion of superoxide dismutase as well as catalase. Additionally, omeprazole inhibited the expression of interleukin-6 and tumor necrosis factor-α. Further, omeprazole inhibited the colistin-induced rise in Bax and the down-regulation of Bcl2 mRNA expression. An assessment of the serum levels of colistin revealed that omeprazole had no significant impact. However, it was observed that omeprazole significantly inhibited the accumulation of colistin in kidney tissues. In conclusion, omeprazole protects against colistin-induced nephrotoxicity. This can be attributed to, at least partly, omeprazole’s anti-oxidant, anti-inflammatory and anti-apoptotic activities in addition to its ability to prevent the toxic accumulation of colistin in kidneys.
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&NA;. "Omeprazole see Furosemide/omeprazole." Reactions Weekly &NA;, no. 354 (June 1991): 11. http://dx.doi.org/10.2165/00128415-199103540-00049.
Повний текст джерела
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Javed, Mamoona, Muhammad Hayder Ali, Muhammad Saad Tanveer, and Muhammad Hassan Tanveer. "Omeprazole vs Lansoprazole in the Management of Gastroesophageal Reflux Disease: A Systematic Literature Review." Journal of Medical Research and Innovation 4, no. 2 (March 29, 2020): e000204. http://dx.doi.org/10.32892/jmri.204.
Повний текст джерелаАнотація:
Objective: To evaluate the effectiveness and safety of omeprazole compared to lansoprazole in Gastroesophageal reflux disease patients (GERD).
Methods: A systematic search of MEDLINE, EMBASE (inception to December 2019) and CENTRAL (January 2011 to December 2019) was conducted to identify the relevant articles. A detailed inclusion-exclusion criterion was developed and implemented to screen the abstracts. Full texts of the selected abstracts were then assessed to establish their inclusion or exclusion in our review. Cochrane risk of bias criterion was used to assess the methodological quality of the included studies. All relevant data were extracted and the results were summarised narratively.
Results: 9 studies met our inclusion-exclusion criteria and were included in this review. In all three trials reporting on heartburn and regurgitation, both omeprazole and lansoprazole were found to be effective in relieving the symptoms of heartburn and regurgitation; however, there was no evidence that one is better than the other. Five out of six studies reporting on intragastric pH provided the evidence of omeprazole’s superiority over lansoprazole in controlling gastric pH. Omeprazole lowered intragastric pH faster and the results lasted longer compared to lansoprazole. The results were statistically significant.
Conclusion: There is no significant difference in the clinical effectiveness of omeprazole and lansoprazole in relieving symptoms of heartburn and regurgitation. However, omeprazole is more effective in reducing gastric acidity than lansoprazole.
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Skvortsova, T. A., G. Yu Knorring, and E. N. Kareva. "Use of Omeprazole in Paediatric Patients in Russia." Doctor.Ru 20, no. 10 (2021): 39–43. http://dx.doi.org/10.31550/1727-2378-2021-20-10-39-43.
Повний текст джерелаАнотація:
Objective of the Review: To analyse clinical and pharmacological characteristics and normative documents in the use of modern proton pump inhibitors (PPI) in paediatric patients in the Russian Federation. Key Points. PPIs remain a widely used and efficient therapy of acid-related disorders in children; however, prescription should be based not only on clinical characteristics of a patient, but also on normative documents, e.g., instructions for the use of PPIs in paediatric population for certain indications approved by the Ministry of Health of Russia, since healthcare providers are responsible for off-label prescriptions. Conclusion. Omeprazole is one of the most well-studied PPIs; it has good evidence base for the use in children; however, in Russia, most omeprazoles have contraindications in paediatric population. Omez is indicated for the management of gastroesophageal reflux and duodenal ulcer caused by Helicobacter pylori in children. Keywords: acid-related disorders, children, paediatrics, proton pump inhibitors, Omeprazole.
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&NA;. "Omeprazole." Reactions Weekly &NA;, no. 1382 (December 2011): 28. http://dx.doi.org/10.2165/00128415-201113820-00100.
Повний текст джерела
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&NA;. "Omeprazole." Reactions Weekly &NA;, no. 1386 (January 2012): 29–30. http://dx.doi.org/10.2165/00128415-201213860-00102.
Повний текст джерела
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&NA;. "Omeprazole." Reactions Weekly &NA;, no. 1390 (February 2012): 28. http://dx.doi.org/10.2165/00128415-201213900-00108.
Повний текст джерелаДисертації з теми "Omeprazole"
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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.
Повний текст джерелаАнотація:
Orientadores: Nelci Fenalti Hoehr, Alessandra GamberoDissertação (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
2
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.
Повний текст джерелаАнотація:
Orientadores: Cesar Costapinto Santana, Quezia Bezerra CassTese (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
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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/.
Повний текст джерелаАнотація:
O citalopram (CITA), inibidor seletivo da recaptação da serotonina, é disponível na clínica como mistura racêmica dos enantiômeros (+)-(S) e (-)-(R) ou como enantiômero puro (+)-(S)-CITA. O CITA é metabolizado pelo CYP2C19, CYP2D6 e CYP3A ao desmetilcitalopram (DCITA) e pelo CYP2D6 ao didesmetilcitalopram. O estudo investiga a influência de inibidores enzimáticos no metabolismo enantiosseletivo do CITA em ratos e em voluntários sadios. Os ratos machos Wistar (n=6 para cada grupo) foram tratados com dose única de 20 mg/Kg de CITA (grupo controle) ou pré-tratados com 80 mg/Kg de quinidina (grupo quinidina), 10 mg/Kg de fluvoxamina (grupo fluvoxamina) ou 50 mg/Kg de cetoconazol (grupo cetoconazol). As amostras de sangue foram colhidas dos ratos até 20 h após a administração do CITA. Os voluntários sadios fenotipados como metabolizadores extensivos (EM) do CYP2C19 (omeprazol como fármaco marcador), EM do CYP2D6 (debrisoquina como fármaco marcador) e com atividade normal do CYP3A (midazolam como fármaco marcador) receberam dose única p.o. de 20 mg de CITA racêmico associado ou não ao omeprazol (20 mg/dia durante 18 dias). Os enantiômeros do CITA e do DCITA foram analisados no sistema LC-MS/MS, com a coluna quiral Chiralcel OD-R e fase móvel constituída por acetonitrila:metanol:água (30:30:40 v/v/v) contendo 0,05 % de dietilamina. O método foi linear no intervalo de concentrações de 0,1 20 ng de cada enantiômero do CITA e DCITA/mL de plasma humano e de de 0,1 500 ng de cada enantiômero do CITA e DCITA/mL de plasma de rato. Os coeficientes de variação obtidos nos estudos da precisão e a inexatidão foram inferiores a 15 % para plasma humano e plasma de ratos. A disposição cinética do CITA é enantiosseletiva nos ratos dos grupos controle (razão de AUCS/R de 0,4), quinidina (razão de AUCS/R de 0,5) e cetoconazol (razão de AUCS/R de 0,8). A inibição do CYP2D pela quinidina resultou em inibição do metabolismo do CITA e do DCITA de maneira não enantiosseletiva. A inibição do CYP2C pela fluvoxamina e do CYP3A pelo cetoconazol resultou em inibição somente do metabolismo do (+)-(S)-CITA. A disposição cinética do CITA em voluntários sadios é enantiosseletiva na ausência de tratamento com o omeprazol com observação de maior proporção plasmática do enantiômero (-)-(R)-CITA. A razão de AUCS/R obtida para o CITA foi de 0,56 e para o metabólito DCITA foi de 1,06. A administração de CITA racêmico a voluntários sadios em tratamento com o omeprazol exibe perda da enantiosseletividade na farmacocinética do CITA. A razão de AUCS/R foi de 0,96 para o CITA e de 0,92 para o DCITA. A administração de omeprazol em doses múltiplas a voluntários sadios inibe de maneira enantiosseletiva o metabolismo do eutômero (+)-(S)-CITA com aumento das concentrações plasmáticas em aproximadamente 140%.Citalopram (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
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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/.
Повний текст джерелаАнотація:
O nitrito pode ser reduzido a NO de forma dependente do pH ácido do estômago ou por enzimas com atividade nitrito-redutase. O tratamento com omeprazol, previne parte dos efeitos anti-hipertensivos do nitrito administrado por via oral por aumentar o pH gástrico. Contudo, nenhum estudo até o momento avaliou se, assim como o omeprazol, a ranitidina também é capaz de atenuar os efeitos anti-hipertensivos do nitrito de sódio por aumentar o pH gástrico. Nesse estudo, examinamos se a administração oral de ranitidina poderia prejudicar os efeitos anti-hipertensivos do nitrito de sódio administrados por via oral, por interferir na formação de NO e espécies nitrosiladas a partir do nitrito. A fim de verificar a influência da ranitidina no efeito hipotensor do nitrito de sódio, utilizamos animais tratados agudamente com LNAME pré-tratados com ranitidina, omeprazol e veículo e, posteriormente, com nitrito de sódio 15mg/kg. Como esperado, o tratamento com L-NAME resultou em aumento na pressão arterial média (PAM). O pH gástrico foi diferente entre os grupos, tendo um aumento no pH dos animais tratados com ranitidina e omeprazol, quando comparado ao veículo, e os tampões tinham o mesmo pH do veículo e das drogas. O nitrito de sódio exerceu efeitos anti-hipertensivos significativos nos grupos estudados. No entanto, foram observadas menores diminuições na PAM em ratos tratados com omeprazol e ranitidina em comparação aos ratos que receberam veículo. Esses achados foram associados a diminuições nas concentrações gástricas de NO e diminuições nos níveis plasmáticos de espécies nitrosiladas. Além disso, houve aumento nas concentrações de nitrito no estômago. Não foram observadas diferenças nas concentrações de nitrito no plasma. Além disso, não foram observadas diferenças nos níveis de NOx no plasma e estômago entre os grupos do estudo. Os animais tratados com tampão apresentaram resultados similares aos tratados com as drogas. Nossos resultados sugerem que a ranitidina, ao aumentar o pH gástrico, afeta as respostas anti-hipertensivas ao nitrito de sódio oral por diminuir a formação de NO e espécies nitrosiladas. Este fato é reforçado pelo aumento do nitrito no estômago, sugerindo uma diminuição na conversão de nitrito a NO e espécies nitrosiladas no ambiente gástrico.Nitrite 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.
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Jackson, Remonica, Stacy D. Brown, and 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.
Повний текст джерелаАнотація:
Purpose:Omeprazole is a proton pump inhibitor (PPI) used in the treatment of gastrointestinal conditions, such as gastrointestinal esophageal reflux disease (GERD). Omeprazole is often prepared as an oral suspension to accommodate certain patients. Historically, oral suspensions of omeprazole were prepared using pharmaceutical compounding with sodium bicarbonate, but a kit for preparation of omeprazole oral suspension is available, FIRST® - Omeprazole. The purpose of this project is to compare the stability of the active pharmaceutical ingredient (API), omeprazole, in the FIRST® kit product to a traditionally compounded omeprazole suspension, when stored in refrigerated unit-dosed syringes.
Methods: Five 100-mL batches of compounded omeprazole oral suspension (2 mg/mL) and five 300-mL kits of FIRST® - Omeprazole were prepared by a licensed pharmacist, and aliquoted into 5-mL doses in clear luer-lock plastic oral syringes, and stored at refrigerated temperature (2-8oC). Omeprazole concentration was assessed in each batch/kit on the day of preparation. Triplicate syringes from each batch/kit (n = 15 per test group per day) were removed after 7 days, 14 days, 21 days, and 30 days of refrigerated storage. Samples were diluted to assay concentration (1 mg/mL) in ion-free water and filtered using a 0.22-micron microcentrifuge filter tube. Samples were analyzed for omeprazole recovery using a validated high-performance liquid chromatography with ultraviolet detection (HPLC-UV) method. Recovery was quantitatively assessed by comparing sample peak area to a freshly prepared calibration curve (1 – 0.125 mg/mL) using United States Pharmacopoeia (USP) reference standard on each day of sampling. Refrigerator temperatures were recorded daily using a digital thermometer.
Results:Stability was defined as recovery of 90 - 110% of initial concentration of API. For the FIRST® - Omeprazole samples, the chemical potency remained within this window for the entire study period of 30 days. The compounded omeprazole suspension demonstrated a less than 90% average recovery at the day 21 sample. Furthermore, a statistically significant difference in the initial concentration was detected on the day of compounding (p = 0.0244), with the compounded omeprazole starting at 1.89 ± 0.10 mg/mL and the FIRST® - Omeprazole at 1.98 ± 0.04 mg/mL. After 30 days, the compounded omeprazole suspension had an 89.13% average API recovery (standard deviation; ± 5.17%) and the FIRST® - Omeprazole 97.20% API recovery (± 3.59%).
Conclusion:Both traditionally compounded omeprazole suspension (2mg/mL) and FIRST® - Omeprazole suspension (2mg/mL) may be stored in clear luer-lock oral syringes under refrigeration for 14 days, and retain potency between 90 to 110% based on initial concentration. Furthermore, the FIRST® - Omeprazole suspension can be stored for the duration of the product’s beyond-use date of 30 days and retain potency between 90 to 110% of initial concentration or label claim. Finally, the data suggest that API concentration in FIRST® - Omeprazole suspension is more consistent from batch to batch than traditionally compounded omeprazole suspension.
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Gwerder, 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.
Повний текст джерела
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Pinheiro, 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/.
Повний текст джерелаАнотація:
O NO regula diversos sistemas orgânicos. No sistema cardiovascular participa ativamente na regulação do tônus vascular entre outras funções. Disfunções na produção ou disponibilidade de NO podem comprometer sua atuação fisiológica. No âmbito vascular isto pode participar da hipertensão. Além da produção de NO pelas óxido nítrico sintases, outras vias paralela de produção fisiológica de NO a partir do nitrito tem sido descritas. 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, onde o nitrato é excretado na saliva e convertido a nitrito pelas bactérias bucais.Este nitrito é deglutido com a saliva e exerce seus efeitos, através da conversão a NO. 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 redução ocorre principalmente no estômago. Esta tese visa elucidar possíveis mecanismos responsáveis pelos efeitos anti-hipertensivos do nitrito de sódio. Avaliamos ratos 2 rins 1 clipe (2R1C) tratados com nitrito e nitrato e verificamos os efeitos anti-hipertensivo destes. De forma Interessante, o aumento do pH gástrico com omeprazol impediu o efeito anti-hipertensivo tanto do nitrito quanto do nitrato. O omeprazol não gerou qualquer diferença na concentração plasmática de nitrito e nitrato. Foi verificado que o tratamento com nitrito e nitrato resultou em aumento das espécies nitrosiladas no plasma e este aumento foi impedido pelo omeprazol. Também testamos a influência do ciclo entero-salivar no efeito do nitrito e nitrato. Verificamos que o tratamento com enxaguante bucal levou ao bloqueio do efeito anti-hipertensivo do nitrato, mas não alterou este efeito nos animais tratados com nitrito. Em todas as abordagens experimentais o efeito anti-hipertensivo do nitrito apenas ocorreu quando houve aumento da concentração plasmática de espécies nitrosiladas.Nitric 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
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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.
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Introduction: Tacrolimus (TCR) is an immunosuppressant drug widely used in post-transplant organ recipients. Its absorption occurs principally in the duodenum and jejunum, its peak serum concentration is reached between 0.5 and 4 hours after ingestion (average 2 hours), and its absorption may be facilitated by an alkaline medium. Omeprazole (OMP) is a proton pump inhibitor in the parietal cells of the stomach that reaches maximum concentration between 0.5 and 3.5 hours after ingestion (average 2 hours), and because it reduces gastric acidity, it is capable of releasing more alkaline content into the duodenum. Pharmacological interactions between TCR and OMP are always described primarily with respect, to the common metabolic pathway (CYP3A4 and P-gp) used by both medications which may result in elevations of the TCR plasma concentration. The objectives of this study are to identify if there is an increase or decrease in the concentration of tacrolimus when administered after omeprazole and determine the frequency of subjects who increased in two hours, the bioavailability of tacrolimus after using omeprazole. Subjects and Methods: To that end, a double blind, placebo-controlled pilot study was performed in 28 post-renal transplant subjects regularly using TCR (mean: 0.08 ± 0.05 mg/kg/day BID) and OMP (20 mg/day MID). OMP or a placebo was ingested every morning at 6 am after fasting, and TCR was ingested 2 hours later at the doses reported above. Blood samples were taken 2 hours after the ingestion of TCR over 4 consecutive days under both the OMP and placebo regimes, being the subject the control same its. Serum concentrations of TCR were obtained using the chemiluminescent microparticle in human whole blood immunoassay method (CMIA, Abbott Lab., Brazil) after the subjects fasted for 3.5 hours. Results: Of the subjects evaluated, 18 (64.3%) were male, and 10 (35.7%) were female. In total, 8 (28.6%) of subjects received living donor kidneys, and 20 (71.4%) of subjects received cadaveric donor kidneys. The mean age of the subjects was 43 ± 13 years, and the average time since transplant was 41 ± 32 months. The mean serum creatinine and urea levels were 1.6 ± 0.5 mg/dL and 59 ± 27 mg/dL, respectively, and the mean hemoglobin level was 13.7 ± 1.9 g/dL. Conclusion: We found no significant difference in the mean serum TCR concentrations measured under the placebo or OMP regime (15.8 ± 8.7 ng/mL versus 15.7 ± 6.8 ng/mL, respectively, P=0.92). Compared with the placebo period, there was an increase in the serum TCR concentration greater than 10% in 13 subjects and greater than 20% in 10 subjects, which corresponded respectively, to 46.4% and 35.7% of the studied subjects. These data infer that OMP may increase the serum TCR concentration if ingested 2 hours before TCR ingestion, likely through alkalization of the intestinal contents. These frequency rates should be used to calculate the sample sizes needed for future studies with larger numbers of subjects.Introdução: 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
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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.
Повний текст джерелаАнотація:
Orientador: José Eduardo Tanus dos SantosDissertação (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
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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/.
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Úlceras abomasais acarretam diminuição do bem-estar e da produção de leite e carne, porém informações quanto a sua etiopatogenia, diagnóstico, prevenção e tratamento ainda são insuficientes, em especial quando acometem ruminantes adultos. Os protocolos utilizados para prevenção e tratamento desta enfermidade são extrapolados dos determinados para a lesão estomacal em monogástricos, havendo ainda incertezas sobre o efeito dos princípios ativos, doses e vias de administração mais adequados para ruminantes. Com o intuito de testar a capacidade da ranitidina e do omeprazol prevenirem o aparecimento de úlcera abomasal realizou-se administração dos antiácidos concomitantemente ao uso de fenilbutazona por sete dias (4,4 mg/kg, duas vezes ao dia, pela via intravenosa). Oito ovinos hígidos e canulados em abomaso foram distribuídos em dois quadrados latinos 4x4 e tratados com 2 mg de ranitidina/kg de peso vivo, pela via intravenosa, a cada doze horas; 0,4 mg/kg de omeprazol, pela via intravenosa, uma vez ao dia; 4 mg/kg de omeprazol em pasta, via oral, uma vez ao dia; ou nenhum medicamento antiácido (controle). Omeprazol administrado pela via intravenosa desencadeou flebite e maior número de animais apresentou lesões na mucosa abomasal. Omeprazol em pasta não foi eficaz na prevenção de úlcera do tipo 1a. Embora sem diferença entre os grupos, a ranitidina revelou o menor número de animais com lesões confirmadas pelo exame histológico; no entanto, este antagonista H2 ocasionou aumento da frequência cardíaca. O pH e a acidez do conteúdo abomasal, as concentrações séricas do pepsinogênio e da lisozima, bem como a pesquisa de sangue oculto fecal não se mostraram válidos para o diagnóstico da úlcera de abomaso do tipo 1a em ovinos adultos.Abomasal 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.
Книги з теми "Omeprazole"
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Zomorodi, Katayoun. The interaction between omeprazole and diazepam: Investigations performed in various drugmetabolising systems. Manchester: University of Manchester, 1994.
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2
Grant, Okil. Omeprazole. Independently Published, 2018.
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3
Ramy, Jamil. Omeprazole. Independently Published, 2018.
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laid, Jory. Omeprazole. Independently Published, 2018.
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5
Lees, Michelle Anne. Omeprazole usage evaluation. 1992.
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Omeprazole & Acid Inhibition: The Essential Issues - Journal: Digestion, Suppl. 1, 1990 (Omeprazole & Acid Inhibition). S. Karger AG (Switzerland), 1991.
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The Logic of Omeprazole: Treatment by Design. CoMed Communications, 2000.
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Kasiwong, Srirat. Pharmacokinetics of ampicillin, gentamicin, amikacin, and omeprazole in llamas. 1997.
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Stanley, Peter C. Amazon Basic Care Omeprazole: Acid Reducer, Treats Frequent Heartburn. Lulu Press, Inc., 2022.
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Methot, Linda. A drug use evaluation of omeprazole in adult KGH inpatients. 1999.
Знайти повний текст джерелаЧастини книг з теми "Omeprazole"
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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.
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Alarcón, Teresa, Isabel Sánchez Romero, Diego Domingo, Aurora Limia, Francisco De Diaz Rojas, and 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.
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Labenz, J., E. Gyenes, U. Peitz, and 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.
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Labenz, J., E. Gyenes, G. H. Rühl, and 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.
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Dent, J., G. Vantrappen, and 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.
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Festen, H. P. M., H. A. R. E. Tuynman, and 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.
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Dunjić, B. S., J. Axelson, M. S. Dunjić, M. Hashmonai, and 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.
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Lamers, 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.
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Wallmark, 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.
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Owman, C., M. Lindvall-Axelsson, and 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.
Повний текст джерелаТези доповідей конференцій з теми "Omeprazole"
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M.Hussein, Ali, Nadir Nanakali, and 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.
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Gastric ulcer is a chronic condition that occurs when the mucosa of the stomach is broken. There is a physiological equilibrium between aggressive factors and mucosal defense. This study aimed to determine the prevention level and efficiency of herbal medicinal plants (Hypericum perforatum) and compared with the omeprazole drug.Many groups were prepared from Albino male rats, first control group (inoculate with H. pylori and fed with standard pellet), Second group, rats inoculated by H. pylori and prevented with aqueous extract H. perforatum in two dosages (250mg/kg, 500mg/kg), Third group inoculated by H. pylori and prevented with standard drug omeprazole at the dose (20mg/kg).The result showed that H. perforatum inhibits (50.65%) stomach ulcer formation with a high dose. Omeprazole's' group results showed (24.50%) stomachs ulcer formation. Although the result of the current study improves, a high dosage of aqueous extracts of plants has more effectiveness than the low dosage of aqueous extracts of plants.
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Silva, Wilienne Gabriela Torres Da, Nathany França Pessoa, and 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.
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Introdução: A administração de medicamentos por sonda enteral é prática hospitalar comum e os problemas recorrentes estão relacionados às obstruções da sonda. O Omeprazol é um dos mais utilizados é um dos responsáveis por essa obstrução, sendo ele um inibidor da bomba de prótons (inibição específica da enzima H+/K+-ATPase). Objetivo: O objetivo deste trabalho foi fazer uma revisão da literatura quanto a Prescrição e Uso do omeprazol por via de sonda enteral. Material e métodos: Foi feito um levantamento retrospectivo bibliográfico no período de 2017 a 2021, utilizando como base de dados, LILACS(Literatura Latino-Americana e do Caribe em Ciência da Saúde), Scielo (Scientific Eletronic Library Online), PUBMED (National Library of Medicine and The National Institute of Health). Foram utilizadas nos Descritores as seguintes palavras: “Omeprazole” e “Enteral Nutrition”. Os critérios de exclusão foram os trabalhos que não falavam sobre prescrição e uso do omeprazol por sonda. Das bases de dados utilizadas foram encontrados 12 trabalhos, dos quais 4 trabalhos atenderam aos critérios determinados. Resultados: Foram encontrados dados que ao serem analisados mostra que o omeprazol é um dos fármacos mais prescrito para administração via sonda enteral, mesmo não sendo adequado para tal finalidade, por causar a obstrução da sonda pela formação de grânulos, já que sua apresentação na forma de cápsulas duras (20 mg) contém pellets revestidos. Conclusão: Há poucas informações entre os profissionais de saúde sobre o uso de medicações por via sonda, principalmente o omeprazol, que mesmo sendo inadequado na prática clínica continua sendo muito prescrito e utilizado, mostra como é importante a presença de um farmacêutico na equipe multidisciplinar analisando as prescrições para garantir a segurança no uso e administração de fármacos e contribuindo para melhorias na segurança do paciente.
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Silitonga, Hendrika Andriana, Gontar Alamsyah Siregar, Rosita Juwita Sembiring, and 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.
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ABSTRACT Background: Recent studies showed that Interleukin-8 (IL-8), activated cytokine immune response which plays an important role in the development of acute and chronic gastritis. Harmless anti-inflammatory therapeutic alternatives have been proposed, for example, the consumption of Sechium Edule Jacq. Swartz (chayote). Antioxidant (flavonoid) and cell regeneration (alkaloid) agents were found in chayote. This study aimed to determine the effect of chayote Sechium Edule Jacq. Swartz extracts on the level of IL-8 in Wistar rats with aspirin- induced gastritis. Subjects and Method: This was a randomized controlled trial (RCT) conducted at the laboratory of Mathematics and Natural Science, Universitas Sumatra Utara from January to February 2020. A total of 35 male Wistar rats was selected for this study and randomly allocated into 7 groups: (1) Negative control; (2) Positive control; (3) 100 mg/ kg BW chayote ethanol extract ; (4) 200 mg/kg BW chayote ethanol extract; (5) 100 mg/ kg BW chayote ethyl acetate fraction; (6) 200 mg/kg BW chayote ethyl acetate fraction; and (7) 20 mg omeprazole. The rats in positive control and treatment groups were induced with aspirin (200mg/ kg BW). The negative control group received no intervention. The dependent variable was level of IL-8 measured by ELISA. The independent variables were treatment status. The data were analyzed by One Way Anova and post hoc test. Results: The mean differences of IL-8 level were not statistically significant between study groups (p= 0.327). Mean of IL-8 level was higher in positive control group (Mean= 160.80; SD= 6.90) than in negative control group (Mean= 141.20; SD= 10.98). The lowest IL-8 level was in 100mg/ kg BW chayote ethanol extract group (Mean= 149.94; SD= 40.4), followed by 200mg/ kg BW (Mean= 152.4; SD= 30.73) and 100mg/ kg BW (Mean= 164.60; SD= 25.04) chayote ethyl acetate fraction groups, 20 mg omeprazole group (Mean= 170.60; SD= 21.58), and 200 mg/ kg BW chayote ethanol extract group (Mean= 176.80; SD= 10.98). Conclusion: The low dose (100mg/ kg BW) chayote ethanol extract has the most potential antiinflammation effect on in vitro gastritis with the lowest IL-8 level of all doses of chayote ethanol extract, chayote ethyl acetate fraction, and omeprazole. Keywords: antiinflammation, IL-8, chayote ethanol extract, ethyl acetate fraction, omeprazole, aspirin induced gastritis Correspondence: Hendrika Andriana Silitonga. Department of Histology, Faculty of Medicine, Universitas Methodist Indonesia. Email: andr38482@gmail.com. Mobile: +6281361430688. DOI: https://doi.org/10.26911/the7thicph.05.35
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Harrison, B., D. Despain, A. Mandagere, G. Walker, and 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.
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Fatima, S., N. Sheikh, and 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.
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Tangamornsuksan, Wimonchat, Pongpak Thiansupornpong, Thirawut Morasuk, Ornrat Lohitnavy, and 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.
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Catapano, 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.
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BHANOT, 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.
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Conesa Nicolás, E., AM Chica Marchal, AC Viney, S. Nuñez Bracamonte, C. Juez Santamaría, A. Lloret Llorca, B. Fernández-Lobato, CN García Matillas, and 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.
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Patlolla, Jagan Mohan R., Yuting Zhang, Li Qian, Vernon E. Steele, and 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.
Повний текст джерелаЗвіти організацій з теми "Omeprazole"
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Xie, Cheng, Langhui Liu, Suyou Zhu, and 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, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0048.
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