Academic literature on the topic 'Nitric oxide bioavailability'
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Journal articles on the topic "Nitric oxide bioavailability"
Sobolewski, Peter, Irene Gramaglia, John Frangos, Marcos Intaglietta, and Henri C. van der Heyde. "Nitric oxide bioavailability in malaria." Trends in Parasitology 21, no. 9 (September 2005): 415–22. http://dx.doi.org/10.1016/j.pt.2005.07.002.
Full textHEYMAN, SAMUEL N., MARINA GOLDFARB, DAVID DARMON, and MAYER BREZIS. "Tissue Oxygenation Modifies Nitric Oxide Bioavailability." Microcirculation 6, no. 3 (September 1999): 199–203. http://dx.doi.org/10.1111/j.1549-8719.1999.tb00102.x.
Full textSuschek, Christoph V., Dennis Feibel, Maria von Kohout, and Christian Opländer. "Enhancement of Nitric Oxide Bioavailability by Modulation of Cutaneous Nitric Oxide Stores." Biomedicines 10, no. 9 (August 29, 2022): 2124. http://dx.doi.org/10.3390/biomedicines10092124.
Full text&NA;. "Clopidogrel improves nitric oxide bioavailability in CAD." Inpharma Weekly &NA;, no. 1550 (August 2006): 19. http://dx.doi.org/10.2165/00128413-200615500-00050.
Full textPrice, Daniel T., Joseph A. Vita, and John F. Keaney. "Redox Control of Vascular Nitric Oxide Bioavailability." Antioxidants & Redox Signaling 2, no. 4 (December 2000): 919–35. http://dx.doi.org/10.1089/ars.2000.2.4-919.
Full textHuang, K. T., T. H. Han, D. R. Hyduke, M. W. Vaughn, H. Van Herle, T. W. Hein, C. Zhang, L. Kuo, and J. C. Liao. "Modulation of nitric oxide bioavailability by erythrocytes." Proceedings of the National Academy of Sciences 98, no. 20 (September 25, 2001): 11771–76. http://dx.doi.org/10.1073/pnas.201276698.
Full textChen, Jing-yi, Zi-xin Ye, Xiu-fen Wang, Jian Chang, Mei-wen Yang, Hua-hua Zhong, Fen-fang Hong, and Shu-long Yang. "Nitric oxide bioavailability dysfunction involves in atherosclerosis." Biomedicine & Pharmacotherapy 97 (January 2018): 423–28. http://dx.doi.org/10.1016/j.biopha.2017.10.122.
Full textLai, Wai Keung Christopher, and Ming Yin Kan. "Homocysteine-Induced Endothelial Dysfunction." Annals of Nutrition and Metabolism 67, no. 1 (2015): 1–12. http://dx.doi.org/10.1159/000437098.
Full textLiu, Xiaoyu, John Fassett, Yidong Wei, and Yingjie Chen. "Regulation of DDAH1 as a Potential Therapeutic Target for Treating Cardiovascular Diseases." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/619207.
Full textRush, James W. E., Steven G. Denniss, and Drew A. Graham. "Vascular Nitric Oxide and Oxidative Stress: Determinants of Endothelial Adaptations to Cardiovascular Disease and to Physical Activity." Canadian Journal of Applied Physiology 30, no. 4 (August 1, 2005): 442–74. http://dx.doi.org/10.1139/h05-133.
Full textDissertations / Theses on the topic "Nitric oxide bioavailability"
Huang, Kan. "Impact of the short-term consumption of a moderately high fat diet on nitric oxide production and bioavailability." [Huntington, WV : Marshall University Libraries], 2009. http://www.marshall.edu/etd/descript.asp?ref=986.
Full textDobrucki, Iwona T. "Restitution of endothelial function and nitric oxide bioavailability in aging vasculature." Ohio : Ohio University, 2004. http://www.ohiolink.edu/etd/view.cgi?ohiou1107794593.
Full textEvans, Kevin Andrew. "Hypoxia and vascular nitric oxide bioavailability : implications for the pathophysiology of high-altitude illness." Thesis, University of South Wales, 2009. https://pure.southwales.ac.uk/en/studentthesis/hypoxia-and-vascular-nitric-oxide-bioavailability(3cd64bcd-5fb9-4209-a6f3-ab219e906a17).html.
Full textPrisby, Rhonda D., Michael W. Ramsey, Bradley J. Behnke, James M. Dominguez, Anthony J. Donato, Matthew Allen, and Michael D. Delp. "Aging Reduces Skeletal Blood Flow, Endothelium-Dependent Vasodilation and Nitric Oxide Bioavailability in Rats." Digital Commons @ East Tennessee State University, 2009. https://dc.etsu.edu/etsu-works/4142.
Full textPrisby, Rhonda D., Michael W. Ramsey, Bradley J. Behnke, James M. Dominguez, Anthony J. Donato, Matthew R. Allen, and Michael D. Delp. "Aging Reduces Skeletal Blood Flow, Endothelium-Dependent Vasodilation and Nitric Oxide Bioavailability in Rats." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/4130.
Full textGourine, Andrey. "The importance of nitric oxide bioavailability and endothelial mechanisms for cardioprotection by pharmacological intervention during myocardial ischaemia and reperfusion /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-069-9/.
Full textSharma, Arpeeta. "Molecular and pharmacological characterization of mutant (F92A) caveolin-1 : a direction towards increasing nitric oxide bioavailability." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27804.
Full textSouza, Filho Luis Gustavo de 1974. "Efeito da administração aguda e cronica de inibidores das oxido nitrico sintases na infiltração de eosinofilos para as vias aereas de camundongos alergicos." [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308924.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-11T19:38:05Z (GMT). No. of bitstreams: 1 SouzaFilho_LuisGustavode1974-_M.pdf: 2079653 bytes, checksum: 497d01659ac0eed18bd9c81662ca0b59 (MD5) Previous issue date: 2008
Resumo: Os inibidores das óxido nítrico sintases (NOS) são amplamente utilizados para avaliar a contribuição do NO na alergia pulmonar, mas os dados obtidos pela utilização de tais inibidores são controversos. Neste estudo, ensaios farmacológicos, bioquímicos e farmacocinéticos foram realizados para se avaliar os efeitos dos tratamentos agudo e crônico com o inibidor não seletivo da NOS, L-NAME, assim como do inibidor seletivo para NOS induzível (iNOS), aminoguanidina, sobre a inflamação das vias aéreas em camundongos BALB/c desafiados com ovalbumina (OVA). O tratamento crônico com L-NAME (50 e 150 mg/kg/dia, por três semanas) aumentou significativamente o número de eosinófilos no lavado broncoalveolar (LBA) de animais desafiados com ovalbumina (OVA; 0,19 ± 0,02 e 0,34 ± 0,03 x 106células/LBA, respectivamente; P<0,0001) em relação aos não tratados (0,13 ± 0,02 x 106 células/LBA). No parênquima pulmonar, o tratamento crônico com L-NAME (150 mg/kg/dia) também elevou significativamente o número de eosinófilos nos animais desafiados com OVA em relação aos animais não tratados (27,0 ± 5,1 e 18,2 ± 1,6 eosinófilos/brônquio, respectivamente; P<0,05). Contrariamente, os tratamentos agudo com L-NAME (50 mg/kg; gavagem 30 min antes do primeiro desafio com OVA) e crônico com aminoguanidina (20 mg/kg/dia, por três semanas) reduziram o número de eosinófilos no LBA (0,05 ± 0,01 e 0,04 ± 0,02 x 106 células/LBA, respectivamente; P<0,05) em relação ao controle. Os tratamentos agudo e crônico com L-NAME reduziram a atividade da NOS constitutiva (cNOS) no cérebro em relação aos animais não tratados (tratamento agudo: 5,8 ± 0,4 e 3,6 ± 0,2 pmol/min/mg de proteína; tratamento crônico: 5,7 ± 0,3 e 0,7 ± 0,2 pmol/min/mg de proteína, para controle e tratado, respectivamente; P<0,05). A atividade da NOS induzível (iNOS) pulmonar foi significativamente reduzida pelos tratamentos agudo com L-NAME e crônico com aminoguanidina (0,7 ± 0,05 e 0,04 ± 0,02 pmol/min/mg de proteína, respectivamente; P<0,05) em relação aos animais não tratados (1,2 ± 0,2 pmol/min/mg de proteína). Contudo, o tratamento crônico com L-NAME não afetou a atividade da iNOS pulmonar. Os níveis séricos de IgE mostraram-se elevados nos animais desafiados com OVA, mas não foram afetados por nenhum dos tratamentos. O tratamento crônico com aminoguanidina (mas não o tratamento crônico com L-NAME) reduziu os níveis elevados de eotaxina no LBA (3,4 ± 1,2 e 1,0 ± 0,5 pg/ml, para controle e tratado, respectivamente; P<0,05). As reduções dos níveis de NOx no LBA pelos tratamentos agudo com L-NAME e crônico com aminoguanidina (1,8 ± 0,4 e 0,6 ± 0,3 µM, respectivamente) foram maiores quando comparadas ao tratamento crônico com L-NAME (6,8 ± 0,6 µM) em relação aos animais não tratados (8,8 ± 0,8 µM). Os protocolos farmacocinéticos mostraram que o L-NAME não é biodisponível quando dado via oral. As concentrações séricas do metabólito do L-NAME, N?-nitro-L-arginina, diminuiram progressivamente de 30 min a 24 horas após a administração (72,0 a 32,1 ng/mL). No tratamento crônico com L-NAME, a concentração do N?-nitro-L-arginina (16,2 ng/mL) mostrou-se próxima do limite de detecção do método (10 ng/ml). Em conclusão, o tratamento crônico com L-NAME por três semanas produziu baixas concentrações séricas do N?-nitro-L-arginina, causando inibição preferencial da atividade da cNOS. Portanto, a potenciação do influxo de eosinófilos pelo tratamento crônico com L-NAME supostamente remove o NO protetor derivado da cNOS, com nenhuma interferência sobre o agravamento da inflamação devido ao NO oriundo da iNOS
Abstract: Nitric oxide synthase (NOS) inhibitors are largely used to evaluate the NO contribution to pulmonary allergy, but contrasting data have been obtained. In this study, pharmacological, biochemical and pharmacokinetic studies were performed to evaluate the effects of acute and chronic treatment of BALB/C mice with non-selective (L-NAME) and selective (aminoguanidine) NOS inhibitors in ovalbumin (OVA)-challenged mice. Long-term L-NAME treatment (50 and 150 mg/kg/day, three weeks) significantly increased the eosinophil number in bronchoalveolar lavage (BAL) fluid (0.19 ± 0.02 and 0.34 ± 0.03 x 106 cells / BAL, respectively; P<0.0001) in comparison with non-treated animals (0.13 ± 0.02 x 106 cells / BAL). In the bronchiolar parenchyma, chronic L-NAME treatment (150 mg/kg/day) also increased the eosinophil number (18.2 ± 1.6 and 27.0 ± 5.1 eosinophils/bronchio, for treated and untreated, respectively; P<0.05). On the other hand, acute L-NAME (50 mg/kg, given by gavage 30 min prior to the first OVA challenge) and aminoguanidine (20 mg/kg/day, three weeks) rather reduced the eosinophil number (0.05 ± 0.0 and 0.04 ± 0.02 x 106 cells / BAL, respectively; P<0.05). Chronic and acute L-NAME treatments markedly reduced the constitutive NOS (cNOS) activity in brain (0.7 ± 0.2 and 3.6 ± 0.2 pmol/min/mg of protein, respectively; P<0.05) in comparison with untreated animals (5.7 ± 0.3 and 5.8 ± 0.4 pmol/min/mg of protein, respectively). The inducible pulmonary NOS (iNOS) activity was markedly reduced by acute L-NAME and aminoguanidine (0.7 ± 0.05 and 0.04 ± 0.02 pmol/min/mg of protein, respectively; P<0.05) compared with untreated animals (1.2 ± 0.2 pmol/min/mg of protein). In contrast, chronic L-NAME failed to affect the iNOS activity. The increased serum IgE levels seen in OVA-challenged animals were not affected by any treatment. Aminoguanidine (but not chronic L-NAME) restored the increased eotaxin levels in BAL (3.4 ± 1.2 and 1.0 ± 0.5 pg/ml; P<0.05). The NOx- levels in BAL fluid were reduced by both acute and chronic L-NAME, as well as by aminoguanidine (1.8 ± 0.4, 6.8 ± 0.6 and 0.6 ± 0.3 µM, respectively; P<0.05) compared with untreated animals (8.8 ± 0.8 µM); however, the reductions of NOx- levels by acute L-NAME and aminoguanidine were significantly higher than the chronic L-NAME treatment. The pharmacokinetic protocols showed that L-NAME per se is not bioavailable when given per os. The serum concentrations of its metabolite N?-nitro-L-arginine decreased from 30 min to 24 h (72.0 to 32.1 ng/mL) after acute L-NAME intake. In chronic treatment, N?-nitro-L-arginine concentration (16.2 ng/mL) was close to the detection limit (10 ng/mL). In conclusion, 3-week treatment with L-NAME yields low serum N?-nitro-L-arginine concentrations, causing a preferential inhibition of cNOS activity. Therefore, potentiation of eosinophil influx by chronic L-NAME reflects a removal of protective cNOS-derived NO, with no interference on the ongoing inflammation due to iNOS-derived NO
Mestrado
Mestre em Farmacologia
Koegelenberg, Anna Susanna Elizabeth. "The relationship between pre-diabetic hyperglycemia and markers of nitric oxide bioavailability in a cohort of Africans and Caucasians : the SABPA-study / Anna Susanna Elizabeth Koegelenberg." Thesis, North-West University, 2012. http://hdl.handle.net/10394/8708.
Full textThesis (MSc (Physiology))--North-West University, Potchefstroom Campus, 2013
"New Approaches For The Treatment Of Erectile Dysfunction In Conditions Of Low Nitric Oxide Formation Or Bioavailability: Investigation Of Rho-kinase Inhibitors And Soluble Guanylate Cyclase-targeted Therapies." Tulane University, 2014.
Find full textacase@tulane.edu
Book chapters on the topic "Nitric oxide bioavailability"
Zoccali, Carmine. "Endothelial Dysfunction, Nitric Oxide Bioavailability, and Asymmetric Dimethyl Arginine." In Cardiorenal Syndrome, 235–44. Milano: Springer Milan, 2010. http://dx.doi.org/10.1007/978-88-470-1463-3_17.
Full textFried, Robert, and Richard M. Carlton. "The Beneficial Effect of Omega-3 PUFA and L-Arginine on Endothelial Nitric Oxide (NO) Bioavailability." In Flaxseed, 45–65. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/b22986-3.
Full textDemosthenous, Michael, Konstantinos Triantafyllou, and Nikolaos Koumallos. "Takotsubo Syndrome and Nitric Oxide Bioavailability." In Differential Diagnosis of Chest Pain. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.92235.
Full textHuang, Annong, Shane R. Thomas, and John F. Keaney. "Measurements of redox control of nitric oxide bioavailability." In Methods in Enzymology, 209–16. Elsevier, 2002. http://dx.doi.org/10.1016/s0076-6879(02)59185-0.
Full textKobayashi, Jun. "Nitric Oxide Bioavailability and Insulin Resistance: An Overview." In Challenges and Advances in Pharmaceutical Research Vol. 8, 79–95. Book Publisher International (a part of SCIENCEDOMAIN International), 2022. http://dx.doi.org/10.9734/bpi/capr/v8/4440a.
Full textPei, Zhe, Kuo-Chieh Lee, Amber Khan, and Hoau-Yan Wang. "Brain Insulin Resistance, Nitric Oxide and Alzheimer’s Disease Pathology." In The Role of Nitric Oxide in Type 2 Diabetes, 238–59. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010014.
Full textYousefzadeh, Nasibeh, Sajad Jeddi, Khosrow Kashfi, and Asghar Ghasemi. "Role of Nitric Oxide in Type 2 Diabetes-Induced Osteoporosis." In The Role of Nitric Oxide in Type 2 Diabetes, 161–89. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010011.
Full textBahadoran, Zahra, Mattias Carlström, Parvin Mirmiran, and Asghar Ghasemi. "Asymmetrical Dimethyl Arginine, Nitric Oxide, and Type 2 Diabetes." In The Role of Nitric Oxide in Type 2 Diabetes, 67–86. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010007.
Full textFried, Robert. "Asymmetric Dimethylarginine Impairs Nitric Oxide Bioavailability and Jeopardizes Cardio-Sexual Function." In Erectile Dysfunction As a Cardiovascular Impairment, 181–202. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-420046-3.00006-8.
Full textRanjbar, Tara, Jennifer L. O’Connor, and Khosrow Kashfi. "Therapeutic Management of Type 2 Diabetes: The Nitric Oxide Axis." In The Role of Nitric Oxide in Type 2 Diabetes, 210–37. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010013.
Full textConference papers on the topic "Nitric oxide bioavailability"
Yifru, T., T. Matlock, A. Hudler, S. Ye, F. Holguin, and D. E. Winnica. "Restoration of Nitric Oxide Bioavailability Decreases Parkin Expression in Airway Epithelial Cells." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3237.
Full textCho, J., P. Witting, M. Verma, TC Amis, and JR Wheatley. "Reduction of Endothelial Nitric Oxide Bioavailability in Carotid Arteries Exposed to Snoring-Like Vibratory Energy." 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.a3984.
Full textWatanabe, T., M. Ishikawa, K. Abe, T. Ishikawa, S. Imakiire, T. Ohtsubo, K. Kaneko, T. Fukuuchi, and H. Tsutsui. "Hyperuricemia Impaired Nitric Oxide Bioavailability and Deteriorated Pulmonary Arterial Hypertension in Xanthine Oxidoreductase (XOR)-Independent Manner in Rats." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7843.
Full textGraham, Drew A., Danil V. Dobrynin, Alexander Fridman, Gary Friedman, and Alisa Morss Clyne. "A Pin-to-Hole Spark Discharge Plasma Generates Nitric Oxide and Can Be Safely Applied to an Endothelial Cell Monolayer." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206764.
Full textElshiekh, Duaa Ibnomer, Hadeel Hendawi, Aya Goul, Dina Awartan, Isra Marei, Christopher Triggle, and Haissam Abou Saleh. "Effect of Hyperglycemia on eNOS function in EPCs." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0215.
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