Relevant bibliographies by topics / Nitric oxide bioavailability

Academic literature on the topic 'Nitric oxide bioavailability'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Nitric oxide bioavailability"

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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.

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HEYMAN, 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.

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Suschek, 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.

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The generation of nitric oxide (NO) in the skin plays a critical role in wound healing and the response to several stimuli, such as UV exposure, heat, infection, and inflammation. Furthermore, in the human body, NO is involved in vascular homeostasis and the regulation of blood pressure. Physiologically, a family of enzymes termed nitric oxide synthases (NOS) generates NO. In addition, there are many methods of non-enzymatic/NOS-independent NO generation, e.g., the reduction of NO derivates (NODs) such as nitrite, nitrate, and nitrosylated proteins under certain conditions. The skin is the largest and heaviest human organ and contains a comparatively high concentration of these NODs; therefore, it represents a promising target for many therapeutic strategies for NO-dependent pathological conditions. In this review, we give an overview of how the cutaneous NOD stores can be targeted and modulated, leading to a further accumulation of NO-related compounds and/or the local and systemic release of bioactive NO, and eventually, NO-related physiological effects with a potential therapeutical use for diseases such as hypertension, disturbed microcirculation, impaired wound healing, and skin infections.
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&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.

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Price, 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.

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Huang, 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.

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Chen, 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.

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Lai, 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.

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This review discussed and in particular emphasis the potential cellular pathways and the biological processes involved that lead to homocysteine-induced endothelial dysfunction, in particular in the impaired endothelial dependent dilatation aspect. Hyperhomocysteinemia is an independent cardiovascular risk factor that has been associated with atherosclerotic vascular diseases and ischemic heart attacks. The potential mechanisms by which elevated plasma homocysteine level leads to reduction in nitric oxide bioavailability include the disruptive uncoupling of nitric oxide synthase activity and quenching of nitric oxide by oxidative stress, the enzymatic inhibition by asymmetric dimethylarginine, endoplasmic reticulum stress with eventual endothelial cell apoptosis, and chronic inflammation/prothrombotic conditions. Homocysteine-induced endothelial dysfunction presumably affecting the bioavailability of the potent vasodilator ‘nitric oxide', and such dysfunction can easily be monitor by flow-mediated dilation method using ultrasound. Understanding the mechanisms by which plasma homocysteine alter endothelial nitric oxide production is therefore essential in the comprehension of homocysteine-induced impairment of endothelial dependent dilatation, and its association of cardiovascular risk and its pathophysiology.
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Liu, 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.

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Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor that blocks nitric oxide production, while congestive heart failure is associated with increased plasma and tissue ADMA content. Increased plasma ADMA is a strong and independent predictor of all-cause mortality in the community and the strongest predictor of mortality in patients after myocardial infarction. Recent studies demonstrated that dimethylarginine dimethylaminohydrolase-1 (DDAH1) is the critical enzyme for ADMA degradation and thereby plays an important role in maintaining cardiovascular nitric oxide bioavailability. Interestingly, activation of the farnesoid X receptor (FXR) through the bile acid ursodeoxycholic acid (UDCA) or synthetic FXR agonists, such as GW4064, can increase DDAH1 expression. Thus, modulating DDAH1 activity through FXR receptor agonists such as UDCA could be a therapeutic target for treating reduced nitric oxide bioavailability in congestive heart failure and other cardiovascular diseases.
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Rush, 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.

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Cardiovascular disease is the single leading cause of death and morbidity for Canadians. A universal feature of cardiovascular disease is dysfunction of the vascular endothelium, thus disrupting control of vasodilation, tissue perfusion, hemostasis, and thrombosis. Nitric oxide bioavailability, crucial for maintaining vascular endothelial health and function, depends on the processes controlling synthesis and destruction of nitric oxide as well as on the sensitivity of target tissue to nitric oxide. Evidence supports a major contribution by oxidative stress-induced destruction of nitric oxide to the endothelial dysfunction that accompanies a number of cardiovascular disease states including hypertension, diabetes, chronic heart failure, and atherosclerosis. Regular physical activity (exercise training) reduces cardiovascular disease risk. Numerous studies support the hypothesis that exercise training improves vascular endothelial function, especially when it has been impaired by preexisting risk factors. Evidence is emerging to support a role for improved nitric oxide bioavailability with training as a result of enhanced synthesis and reduced oxidative stress-mediated destruction. Molecular targets sensitive to the exercise training effect include the endothelial nitric oxide synthase and the antioxidant enzyme superoxide dismutase. However, many fundamental details of the cellular and molecular mechanisms linking exercise to altered molecular and functional endothelial phenotypes have yet to be discovered. The working hypothesis is that some of the cellular mechanisms contributing to endothelial dysfunction in cardiovascular disease can be targeted and reversed by signals associated with regular increases in physical activity. The capacity for exercise training to regulate vascular endothelial function, nitric oxide bioavailability, and oxidative stress is an example of how lifestyle can complement medicine and pharmacology in the prevention and management of cardiovascular disease. Key words: exercise, artery, reactive oxygen species, antioxidant, hypertension
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Dissertations / Theses on the topic "Nitric oxide bioavailability"

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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.

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Dobrucki, 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.

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Evans, 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.

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Introduction: Nitric oxide (NO) is an integral molecule implicated in the control of vascular function. It has been suggested that vascular dysfunction may lead to the development of acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE), though data to date remains scarce. Therefore, there is a clear need for further work to address the role of NO in the pathogenesis of high-altitude illness. Aims: There were two primary aims of the current work: (1) To examine whether hypoxia mediated changes in systemic NO metabolism are related to the development of AMS and sub-clinical pulmonary oedema and (2) to examine whether hypoxia mediated changes in the trans-cerebral exchange kinetics of NO metabolites are related to the development of AMS and headache. Hypothesis: We hypothesise that hypoxia will be associated with an increase in reactive oxygen species (ROS) formation, resulting in a decrease in vascular NO bioavailability (O2•- + NO → ONOO•-, k = 109 M.s-1). The reduction in NO will lead to vascular dysfunction and impaired oxygen (O2) delivery. Subsequent hypoxaemia will result in pulmonary vascular vasoconstriction and the development of sub-clinical pulmonary oedema within and mild brain swelling. Symptoms and reductions in NO bioavailability will be more pronounced in those who develop AMS since they are typically more hypoxaemic. Alternatively, a hypoxia mediated increase in NO, during vasodilatation, specifically across the cerebral circulation, may activate the trigminovascular system resulting in headache and by consequence, AMS. Methods: Study 1 – AMS symptoms, systemic venous NO concentration and nasal potential difference (NPD), used as a surrogate biomarker of extravascular lung oedema, were quantified in normoxia, after a 6hr passive exposure to 12% oxygen (O2) and immediately following a hypoxic maximal exercise challenge (≈6.5 hrs). Final measurements were 2 obtained two hours into (hypoxic) recovery. Study 2 – AMS, radial arterial and internal jugular venous NO metabolite concentrations and global cerebral blood flow (CBF), using the Kety-Schmidt technique, were assessed in normoxia and after a 9hr passive exposure to 12.9% O2. AMS was diagnosed if subjects presented with a combined Lake Louise score of ≥5 points and an Environmental Symptoms Questionnaire – Cerebral score of ≥0.7 points. Results: Hypoxia was associated with a reduction in total plasma NO, primarily due to a reduction in nitrate (NO3•) and a compensatory increase in red blood cell (RBC)-bound NO(P < 0.05 vs. normoxia) in both studies. Study 1 – Exercise reduced plasma nitrite (NO2•) (P< 0.05 vs. normoxia) whereas RBC-bound NO did not change. NO was not different in those who developed AMS (AMS+) compared to those who remained comparatively more healthy (AMS-) (P < 0.05). NPD was not affected by hypoxia or exercise and was not different between AMS+ and AMS- (P > 0.05). Study 2 – Hypoxia decreased arterial concentration of total plasma NO due primarily to a reduction in NO2•- and nitrate (NO3•-). Hypoxia did not alter the cerebral metabolism of RSNO, whereas the formation of RBC-bound NO increased. Discussion: These findings suggest that alterations in systemic or trans-cerebral NO metabolism are not implicated in the pathophysiology of AMS or sub-clinical pulmonary oedema. However, hypoxia was associated with an overall reduction in the total NO pool (NOx), whereas, selected alterations in more vasoactive NO metabolites were observed. Reductions in the partial pressure of O2 (pO2) were thought to be a key regulator in these changes. Overall net increases in RBC NO and corresponding reductions in plasma NO2• in the face of no alterations in NOx indicates that rather than being simply consumed, NO is reapportioned to other NO metabolites and this may be implicated in the pathophysiology of AMS.
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Prisby, 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.

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Introduction: Aging has been shown to diminish bone blood flow in rats and humans. The purpose of this study was to determine whether blood flow to regions of the femur perfused primarily through the principal nutrient artery (PNA) are diminished with aging and whether this putative reduction in flow is associated with impaired endothelium‐dependent vasodilation. Materials and Methods: Blood flow was measured in conscious young adult (4–6 mo old) and aged (24–26 mo old) male Fischer‐344 rats using radiolabeled microspheres. Endothelium‐dependent vasodilation of the PNA was assessed in vitro using acetylcholine (ACh), whereas the contribution of the NO synthase (NOS) and cyclooxygenase (COX) signaling pathways to endothelium‐dependent vasodilation was determined using the NOS and COX inhibitors L‐NAME and indomethacin, respectively. Results: Femoral blood flow in the aged rats was 21% and 28% lower in the proximal and distal metaphyses, respectively, and 45% lower in the diaphyseal marrow. Endothelium‐dependent vasodilation was reduced with old age (young: 83 ± 6% maximal relaxation; aged: 62 ± 5% maximal relaxation), whereas endothelium‐independent vasodilation (sodium nitroprusside) was unaffected by age. The reduction in endothelium‐dependent vasodilation was mediated through impairment of the NOS signaling pathway, which resulted in lower NO bioavailability (young: 168 ± 56 nM; aged: 50 ± 7 nM). Conclusions: These data show that reductions in metaphyseal bone and diaphyseal marrow perfusion with old age are associated with diminished endothelium‐dependent vasodilation through an impairment of the NOS mechanism. Such age‐related changes in bone perfusion and vascular NO signaling could impact clinical bone loss, increase risk of fracture, and impair fracture healing in the elderly.
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Prisby, 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.

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We determined whether aging diminishes bone blood flow and impairs endothelium‐dependent vasodilation. Femoral perfusion was lower in old animals, as well as endothelium‐dependent vasodilation and NO bioavailability. These effects could contribute to old age—related bone loss and the increased risk of fracture. Introduction: Aging has been shown to diminish bone blood flow in rats and humans. The purpose of this study was to determine whether blood flow to regions of the femur perfused primarily through the principal nutrient artery (PNA) are diminished with aging and whether this putative reduction in flow is associated with impaired endothelium‐dependent vasodilation. Materials and Methods: Blood flow was measured in conscious young adult (4–6 mo old) and aged (24–26 mo old) male Fischer‐344 rats using radiolabeled microspheres. Endothelium‐dependent vasodilation of the PNA was assessed in vitro using acetylcholine (ACh), whereas the contribution of the NO synthase (NOS) and cyclooxygenase (COX) signaling pathways to endothelium‐dependent vasodilation was determined using the NOS and COX inhibitors L‐NAME and indomethacin, respectively. Results: Femoral blood flow in the aged rats was 21% and 28% lower in the proximal and distal metaphyses, respectively, and 45% lower in the diaphyseal marrow. Endothelium‐dependent vasodilation was reduced with old age (young: 83 ± 6% maximal relaxation; aged: 62 ± 5% maximal relaxation), whereas endothelium‐independent vasodilation (sodium nitroprusside) was unaffected by age. The reduction in endothelium‐dependent vasodilation was mediated through impairment of the NOS signaling pathway, which resulted in lower NO bioavailability (young: 168 ± 56 nM; aged: 50 ± 7 nM). Conclusions: These data show that reductions in metaphyseal bone and diaphyseal marrow perfusion with old age are associated with diminished endothelium‐dependent vasodilation through an impairment of the NOS mechanism. Such age‐related changes in bone perfusion and vascular NO signaling could impact clinical bone loss, increase risk of fracture, and impair fracture healing in the elderly.
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Gourine, 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/.

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Sharma, 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.

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Nitric Oxide (NO) produced by the endothelium is a critical mediator of vascular function and plays an important role in the protection against various cardiovascular diseases1. In fact, a central feature of most cardiovascular diseases is reduced bioavailability of NO resulting from impaired endothelial function. Consequently, therapies that improve NO synthesis and availability in disease settings are relevant. Endothelial nitric oxide synthase (eNOS) is a membrane enzyme expressed exclusively in vascular endothelial cells and is responsible for NO production. Improper regulation of the enzyme results in production of eNOS-derived superoxide anion (O₂₋) instead of NO. O₂₋ is an oxidative stress mediator and scavenges NO, thereby contributing to lowered NO bioavailability. Extensive research has demonstrated a number of factors involved in positively regulating eNOS activity. However, one of the few proteins that bind to eNOS under basal conditions and inhibit NO release is Caveolin-1 (Cav-1), the major coat protein of plasma membrane lipid-enriched invaginations known as caveolae². Recently, it was demonstrated that a single amino acid substitution of the Cav-1 protein, mutant known as F92A Cav-1, is unable to inhibit eNOS³. Furthermore, preliminary data indicates that high expression of F92A Cav-1 can increase basal NO release. Due to the significance of NO in vascular function, the current work explores the possible mechanisms by which F92A Cav-1 potentiates eNOS activity and NO release. We report that F92A Cav-1 preserves the unique properties of Cav-1, including targeting to caveolae and forming high molecular weight oligomers, which are essential for caveolae organelle biogenesis. Moreover, F92A Cav-1 still retains the ability to bind to eNOS without altering its subcellular localization, indicating that F92A Cav-1 can prevent eNOS binding to endogenous Cav-1, which could rationalize the increased NO release observed. Lastly, we provide evidence that over-expression of F92A Cav-1 reduces the release of basal O₂₋ in endothelial cells as compared to WT Cav-1, revealing another potential positive effect of the mutant Cav-1. Hence, this report compares the biological properties of WT and F92A Cav-1 and the data collected is aimed at describing a therapeutically relevant pharmacological target to increase NO bioavailability in cardiovascular disease settings.
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Souza, 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.

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Orientador: Edson Antunes
Dissertação (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
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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.

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Motivation: Cardiovascular disease (CVD) is becoming an eminent health problem worldwide. Several studies have implicated that type 2 diabetes mellitus, together with other risk factors including hypertension, contributes significantly to the development of CVD. Vascular endothelial dysfunction is one of the most common characteristics of diabetes, and involves alterations such as a decrease in nitric oxide (NO) bio-availability. However, endothelial dysfunction is already present in individuals suffering from impaired fasting glucose, more commonly known as pre-diabetes. The International Diabetes Federation estimates that adults living with pre-diabetes by 2030 in sub-Saharan Africa will comprise 9.6% of the population, whereas adults living with diabetes will comprise of 4.3% of the population. The excessive amount of pre-diabetics in sub-Saharan Africa and its association with vascular endothelial dysfunction motivated this study. In order to gain a better understanding of this relationship, we wanted to explore the relationship between pre-diabetic hyperglycemia and markers of NO bio-availability in Africans and Caucasians residing in South Africa. Aim: Our aim was firstly to determine whether glucose measures (fasting glucose and glycated hemoglobin (HbA1c)) and markers of NO bio-availability (namely L-arginine, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), L-citrulline and reactive oxygen species (ROS)) differ between African and Caucasian individuals. Secondly, we aimed to determine the relationship of glucose measures with markers of NO bio-availability; blood pressure and renal function. Thirdly we aimed to establish whether these associations are ethnic-specific. Methodology: This study forms part of the SABPA (Sympathetic Activity and Ambulatory Blood Pressure in Africans) study which included a total of 409 urbanised African and Caucasian teachers between the ages of 25 and 65 years. Exclusion criteria were an elevated ear temperature, psychotropic substance dependence or abuse, the use of α- and β-receptor blockers, being blood donors or having been vaccinated during the previous three months. For this substudy participants were excluded due to missing data on HbA1c and markers of NO bioavailability (n=16), participants infected with the human immunodeficiency virus (HIV) (n=19), participants with HbA1c levels greater than or equal to 6.5% (n=29), and participants using diabetes medication (n=5). The overall sample of this study therefore consisted of 340 participants divided into African (n=148) and Caucasian (n=192) sub-groups. All participants signed informed consent forms. The Ethics Review Board of the North-West University approved the study. General health questionnaires were used to determine medication use and lifestyle habits. Anthropometric measurements such as weight, height, and waist circumference were determined. Ambulatory blood pressure measurements (ABPM) and physical activity were monitored during a normal working day. Blood samples were taken after subjects were requested to fast overnight. Biochemical analyses of HbA1c, glucose, Larginine, ADMA, L-citrulline, SDMA, ROS, ferric reducing antioxidant power (FRAP), urea, lipid profile (high-density lipoprotein cholesterol, total cholesterol), γ-glutamyl transferase (GGT), cotinine, high sensitivity C-reactive protein (CRP), and creatinine were performed. HIV testing was performed with First Response HIV Card Test 1-2.0 (PMC Medical, India Pvt Ltd) and confirmed with Pareekshak HIV Triline (UCB Pharma). Results: In our study we found higher levels of L-arginine (p<0.001) in Africans. L-citrulline (p=0.053) levels tended to be higher in Africans who also presented with higher levels of HbA1c (p<0.001), blood pressure (p<0.001) and albumin-to-creatinine ratio (ACR) (1.04 [0.35; 3.95] vs. 0.34 [0.09; 1.88] for Africans and Caucasians, respectively). The Caucasians presented higher levels of SDMA (p<0.001) whereas the groups had similar ADMA and ROS levels. Another finding was the disparate manner in which components of the NO biosynthesis pathway correlated with glucose and HbA1c in both the Africans and Caucasians. In Africans alone, L-citrulline was independently associated with fasting glucose (R2=0.21; β=0.19; p=0.017) and HbA1c (R2=0.21; β=0.19; p=0.018) whereas in Caucasians alone, ADMA was independently associated with fasting glucose (R2=0.13; β=0.39; p<0.001) and HbA1c (R2=0.06; β=0.17 p=0.03). Independent variables included: age, gender, BMI, physical activity, cotinine, GGT, CRP, triglycerides, fasting glucose or HbA1c and systolic blood pressure. Secondly, blood pressure and estimated creatinine clearance were differentially associated with glucose and HbA1c among the two ethnic groups. Independent variables for this model included: age, gender, BMI, physical activity, cotinine, GGT, CRP, triglycerides, fasting glucose or HbA1c and anti-hypertensive medication. Systolic blood pressure was positively associated with fasting glucose (borderline significant relationship p=0.06) and HbA1c (p=0.04) in Caucasians. Glucose was also positively associated with diastolic blood pressure in Caucasians (p=0.008). In Africans alone, estimated creatinine clearance was negatively associated with glucose (borderline significant relationship p=0.088) and HbA1c (p=0.019). A further analysis also showed an independent relationship between estimated creatinine clearance and L-citrulline (R2=0.55; β=-0.20; p=0.0015) in Africans. Conclusion: Regardless of the unfavourable cardiovascular, glucose and renal profile in Africans, they demonstrated a more favourable profile regarding markers of NO bio-availability. Still the main finding remained the lack of associations between markers of NO bio-availability and hyperglycemia in both ethnic groups, with the exception of a positive independent association between L-citrulline and glucose measures in Africans and a positive independent association between ADMA and glucose measures in Caucasians. In the African group, the relationship was probably driven by an unfavourable renal profile, which is characterised by an ACR that is approximately three times higher in Africans than Caucasians. In the Caucasian group, who presented a more favourable cardiovascular profile, our findings support the literature in which hyperglycemia had a significant positive independent association with both ADMA and blood pressure.
Thesis (MSc (Physiology))--North-West University, Potchefstroom Campus, 2013
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"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.

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Nitric oxide (NO) is the principal mediator of erectile function. NO is released from the nerves and endothelium of small arteries in the penis and diffuses into surrounding smooth muscle to vasodilate through activation of soluble guanylate cyclase (sGC). Erectile dysfunction (ED) occurs in 50% of men between the ages of 40 and 70. It is likely that the pathology of ED results from impairment of NO formation or bioavailability in penile tissue. Iatrogenic nerve damage occurring during prostatectomy can attenuate neurotransmission and release of vasodilators from cavernosal nerves. Oxidative stress from chronic conditions such as diabetes and cardiovascular disease generates reactive oxygen species that can oxidize NO and decrease the molecule's bioavailability. The "gold standard" treatment for ED involves use of oral PDE-5 inhibitors that rely on an intact NO-signaling mechanism for efficacy. Although these therapies are easy to use, they are not effective in many patients suffering from ED associated with pathological conditions of decreased NO bioavailability. Rho-kinase inhibitors, sGC stimulators and sGC activators offer three new interventions that may demonstrate efficacy in treating ED associated with low NO bioavailability. Our results suggest that erectile responses to Rho-kinase inhibitors are not modulated by muscarinic receptor blockade, soluble guanylate cyclase inhibition or cavernosal nerve injury in the rat and that Rho-kinase inhibitors are additive and do not potentiate the endogenous NO-mediated erectile response. Our results with BAY 41-8543 show that this sGC stimulator has significant erectile activity and can potentiate erectile responses to low levels of exogenous and endogenously released NO. These results suggest that BAY 41-8543 would be useful in the treatment of ED occurring following nerve damage from prostatectomy. The sGC activator BAY 60-2770 has very potent erectile activity that is enhanced significantly in conditions of oxidative stress when erectile responses to endogenous NO or sGC stimulators are severely diminished. In oxidizing conditions erectile activity of sGC activators may be enhanced further with concomitant PDE-5 inhibitor therapy, providing evidence that sGC activators may be used alone and in combination with existing treatments to improve erectile function in patients who are non-responsive to standard therapeutic options for ED.
acase@tulane.edu
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Book chapters on the topic "Nitric oxide bioavailability"

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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.

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Fried, 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.

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Demosthenous, 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.

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Huang, 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.

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Kobayashi, 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.

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Pei, 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.

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Alzheimer’s disease (AD) is a devastating age-related neurodegenerative disease characterized by progressive pathological changes and functional and cognitive impairments. Brain insulin resistance appears to contribute significantly to the pathology and cognitive deficits among several pathological mechanisms. Brain insulin resistance has been demonstrated in animal models of AD and postmortem human brain tissue from patients with AD dementia. Studies conducted in AD models and humans suggest attenuating brain insulin resistance by agents such as glucagon-like peptide1 (GLP-1) analogs and small molecule drug candidate PTI-125 reduces many AD pathologic features and symptoms. Insulin affects NO levels by activating endothelial and neuronal nitric oxide synthase (eNOS, nNOS), and systemic insulin resistance has been linked to reduced nitric oxide (NO) bioavailability. Increasing NO availability reduces systemic insulin resistance, and the insulin signaling pathway is associated with the activation of eNOS, implying a causal relationship. This chapter explores this relationship and the role of impaired NO availability in brain insulin resistance in AD dementia.
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Yousefzadeh, 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.

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Osteoporosis affects 200 million people worldwide. Osteoporosis in subjects with diabetes is called diabetoporosis, and type 2 diabetes (T2D) contributes to and aggravates osteoporotic fractures. Hyperglycemia, insulin resistance, bone vasculature impairment, increased inflammation, oxidative stress, and bone marrow adiposity contribute to a higher incidence of osteoporotic fractures in T2D. Decreased nitric oxide (NO) bioavailability due to lower endothelial NO synthase (eNOS)-derived NO and higher inducible NOS (iNOS)-derived NO is one of the main mechanisms of the diabetoporosis. Available data indicates that T2D increases osteoclast-mediated bone resorption and decreases osteoblast-mediated bone formation, mediated in part by reducing eNOS-derived NO and increasing iNOS-derived NO. NO donors delay osteoporosis and decrease osteoporotic fractures in subjects with T2D, suggesting the potential therapeutic implication of NO-based interventions for diabetoporosis.
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Bahadoran, 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.

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Asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of nitric oxide (NO) synthase (NOS) isoenzymes, can substantially inhibit vascular NO production at concentrations that are observed in pathophysiological conditions. Over-production of ADMA (via overexpression and/or activity of class 1 of the protein arginine methyltransferases, PRMT-1) alongside decreased catabolism (due to decreased expression and/or activity of dimethylarginine dimethyloaminohydrolase, DDAH) in type 2 diabetes (T2D) and insulin resistance results in increased circulatory and intracellular ADMA levels. Such pathological elevated ADMA levels lead to a decreased NO bioavailability and the development of diabetes complications, including cardiovascular diseases, nephropathy, and retinopathy; elevated ADMA levels also increase the mortality risk in these patients. Here, we discuss current documents indicating how disrupted ADMA metabolism contributes to the development of T2D and its complications. The role of other endogenous methylarginines, i.e., NGmonomethyl- L-arginine (L-NMMA) and NG, NG′-dimethyl-L-arginine (SDMA) on NO production and T2D are also discussed.
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Fried, 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.

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Ranjbar, 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.

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According to the World Health Organization (WHO), the prevalence of obesity across the globe has nearly tripled since 1975, with 39 million children under the age of 5 being overweight or obese in 2020. Obesity is the most common risk factor for developing type 2diabetes (T2D), which may lead to elevated serum triglycerides, hypertension, and insulin resistance. In the pathogenesis of T2D, there is a reduction in nitric oxide (NO) bioavailability. Restoration of NO levels has been associated with many favorable metabolic effects in T2D. Drugs that potentiate NO levels may have a role in improving T2D-associated adverse effects. Current medications approved for use in the management of T2D include biguanides, thiazolidinediones, sulfonylureas, meglitinides, dipeptidyl peptidase-4 (DPP-4) inhibitors, glucagon-like peptide-1 (GLP- 1) receptor agonists, alpha-glucosidase inhibitors, and sodium-glucose co-transporter 2 (SGLT2) inhibitors. These drugs mitigate the many adverse effects associated with T2D. This chapter discusses these classes of drugs, examines their mechanism of action, and presents evidence that these drugs directly or indirectly modulate NO levels.
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Conference papers on the topic "Nitric oxide bioavailability"

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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.

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Cho, 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.

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Watanabe, 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.

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Graham, 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.

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Endothelial cells line all blood vessels and regulate many homeostatic functions (e.g. platelet aggregation, vascular tone, vascular cell proliferation, leukocyte adhesion) by production of the signaling molecule nitric oxide (NO). NO bioavailability and thus endothelial cell function are compromised in many chronic disease states, including diabetes mellitus and its associated micro- and macrovascular complications (e.g. impaired wound healing and atherosclerosis, respectively) [1]. In the specific case of diabetic wound healing, application of exogenous NO to the diseased tissue may help restore critical NO-mediated processes and could positively impact healing and overall patient health [2]. We have developed a novel pin-to-hole spark discharge plasma device that generates NO and can be applied to cultured endothelial cells with minimal cell injury or death. We propose that this plasma device represents a promising novel method for topical NO application.
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Elshiekh, 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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Type 2 diabetes mullites (T2DM) results in different cardiovascular complications. The main cause of these complications is endothelial dysfunction, which affects the endothelium physiologically and pathologically. The chronic hyperglycemia introduced by T2DM impacts the pivotal enzyme endothelial nitric oxide synthase (eNOS) in terms of phosphorylation and dimerization, which initiates oxidative stress and reduces the bioavailability of the vasodilator nitric oxide. To overcome endothelial dysfunction, endothelial progenitor cells (EPCs) contribute to vascular repair due to their regenerative characteristics. The effects of hyperglycemia on EPCs are understudied. Thus, this study aims to investigate the effects of hyperglycemia on the eNOS/Akt signaling pathway and reactive oxygen species (ROS) formation. Cells were treated with normal glucose (NG, 5.5mM) and high glucose (HG, 25mM) media for 3 & 6 days, and the effect on eNOS and Akt phosphorylation were assessed using western blot. ROS was assessed using CellROX stain following 1 and 3 days of treatment. Results showed that both acute and chronic hyperglycemia showed a trend towards decrease in phosphorylation of eNOS and Akt. In addition, ROS formation was increased following 24hr compared to NG. Further investigations are needed to enhance the capability of BOECs to serve as therapeutic tools in T2DM.
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