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Artykuły w czasopismach na temat „Nitric oxide Pathophysiology”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 8 lutego 2022

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1

Conner, Elaine M., and Matthew B. Grisham. "Nitric Oxide: Biochemistry, Physiology, and Pathophysiology." Methods 7, no. 1 (February 1995): 3–13. http://dx.doi.org/10.1006/meth.1995.1002.

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2

Ghosh, Sudakshina, and Serpil C. Erzurum. "Nitric oxide metabolism in asthma pathophysiology." Biochimica et Biophysica Acta (BBA) - General Subjects 1810, no. 11 (November 2011): 1008–16. http://dx.doi.org/10.1016/j.bbagen.2011.06.009.

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3

Kiechle, Frederick L., and Tadeusz Malinski. "Nitric oxide: Biochemistry, Pathophysiology, and detection." Journal of Pharmacological and Toxicological Methods 32, no. 2 (October 1994): 123. http://dx.doi.org/10.1016/1056-8719(94)90064-7.

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4

Haynes, Virginia, Sarah Elfering, Rachel Squires, Nathaniel Traaseth, Joseph Solien, Adam Ettl, and Cecilia Giulivi. "Mitochondrial Nitric-oxide Synthase: Role in Pathophysiology." IUBMB Life 55, no. 10 (January 1, 2004): 599–603. http://dx.doi.org/10.1080/15216540310001628681.

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5

Cipolla, Marilyn. "Pathophysiology and clinical applications of nitric oxide." Journal of Vascular Surgery 31, no. 6 (June 2000): 1314–15. http://dx.doi.org/10.1067/mva.2000.105886.

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Moncada, S. "A2. Nitric oxide and bioenergetics: Physiology and pathophysiology." Nitric Oxide 17 (2007): 9. http://dx.doi.org/10.1016/j.niox.2007.09.007.

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7

MONCADA, S. "Nitric Oxide in the Vasculature: Physiology and Pathophysiology." Annals of the New York Academy of Sciences 811, no. 1 Atheroscleros (April 1997): 60–69. http://dx.doi.org/10.1111/j.1749-6632.1997.tb51989.x.

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8

Bredt, David S. "Endogenous nitric oxide synthesis: Biological functions and pathophysiology." Free Radical Research 31, no. 6 (January 1999): 577–96. http://dx.doi.org/10.1080/10715769900301161.

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9

Baylis, C., and J. Bloch. "Nitric oxide (NO) in renal physiology and pathophysiology." Nephrology Dialysis Transplantation 11, no. 10 (October 1, 1996): 1955–57. http://dx.doi.org/10.1093/oxfordjournals.ndt.a027078.

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10

Lowe, Duane T. "Nitric Oxide Dysfunction in the Pathophysiology of Preeclampsia." Nitric Oxide 4, no. 4 (August 2000): 441–58. http://dx.doi.org/10.1006/niox.2000.0296.

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11

Kelly, Melanie E. M., and Steven Barnes. "Physiology and Pathophysiology of Nitric Oxide in the Retina." Neuroscientist 3, no. 6 (November 1997): 357–60. http://dx.doi.org/10.1177/107385849700300607.

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12

Groves, PH, and AH Henderson. "Can Nitric Oxide Modify the Pathophysiology of Vascular Injury?" Clinical Science 85, s29 (July 1, 1993): 35P—36P. http://dx.doi.org/10.1042/cs085035pb.

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13

De Vente, J. "The Role of Nitric Oxide in Physiology and Pathophysiology." Journal of Chemical Neuroanatomy 9, no. 4 (December 1995): 302. http://dx.doi.org/10.1016/0891-0618(95)90027-6.

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14

Maeda, Hiroshi, Takaaki Akaike, Masaki Yoshida, and Moritaka Suga. "Multiple functions of nitric oxide in pathophysiology and microbiology: analysis by a new nitric oxide scavenger." Journal of Leukocyte Biology 56, no. 5 (November 1994): 588–92. http://dx.doi.org/10.1002/jlb.56.5.588.

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15

Muscará, Marcelo N., and John L. Wallace. "V. Therapeutic potential of nitric oxide donors and inhibitors." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 6 (June 1, 1999): G1313—G1316. http://dx.doi.org/10.1152/ajpgi.1999.276.6.g1313.

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Nitric oxide is a crucial mediator of gastrointestinal mucosal defense, but, paradoxically, it also contributes to mucosal injury in several situations. Inhibitors of nitric oxide synthesis and compounds that release nitric oxide have been useful pharmacological tools for evaluating the role of nitric oxide in gastrointestinal physiology and pathophysiology. Newer inhibitors with selectivity for one of the isoforms of nitric oxide synthase are even more powerful tools and may have utility as therapeutic agents. Also, agents that can scavenge nitric oxide or peroxynitrite are promising as drugs

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16

Sooranna, SR, NH Morris, and PJ Steer. "Placental nitric oxide metabolism." Reproduction, Fertility and Development 7, no. 6 (1995): 1525. http://dx.doi.org/10.1071/rd9951525.

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There is increasing evidence that nitric oxide (NO) has a role in pregnancy. NO is synthesized from L-arginine by NO synthase (NOS), which can exist either as a calcium-dependent or a calcium-independent isoform of the enzyme. Both isoforms are present in placental villi and the authors have measured NOS activities in tissues from early and term normal, pre-eclamptic and growth-retarded pregnancies. Higher activities were seen in first trimester placental villi than at term. An impairment of NO metabolism occurred in placental villi from pre-eclamptic and growth-retarded pregnancies. Smoking a

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17

Ran, Caroline, Julia M. Michalska, Carmen Fourier, Christina Sjöstrand, Elisabet Waldenlind, Anna Steinberg, and Andrea C. Belin. "Analysis of NOS Gene Polymorphisms in Relation to Cluster Headache and Predisposing Factors in Sweden." Brain Sciences 11, no. 1 (December 31, 2020): 34. http://dx.doi.org/10.3390/brainsci11010034.

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Cluster headache is characterized by activation of the autonomic-trigeminal reflex. Nitric oxide can trigger headaches in patients, and nitric oxide signaling is known to be affected in cluster headache. Based on the hypothesis of nitric oxide being involved in cluster headache pathophysiology we investigated nitric oxide synthases as potential candidate genes for cluster headache. We analyzed eight variants in the three forms of nitric oxide synthase (NOS) genes, inducible NOS (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS), and tested for association with cluster headache. Swedish clu

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18

Kudlow, P., D. S. Cha, A. F. Carvalho, and R. S. McIntyre. "Nitric Oxide and Major Depressive Disorder: Pathophysiology and Treatment Implications." Current Molecular Medicine 16, no. 2 (February 4, 2016): 206–15. http://dx.doi.org/10.2174/1566524016666160126144722.

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19

Guix, F. X., I. Uribesalgo, M. Coma, and F. J. Muñoz. "The physiology and pathophysiology of nitric oxide in the brain." Progress in Neurobiology 76, no. 2 (June 2005): 126–52. http://dx.doi.org/10.1016/j.pneurobio.2005.06.001.

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20

ÄAUNGGÅARRD, ERIK. "Physiology and pathophysiology of the L-arginine-nitric oxide pathway." Acta Anaesthesiologica Scandinavica 39 (June 1995): 57. http://dx.doi.org/10.1111/j.1399-6576.1995.tb04271.x.

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21

Cohen, Jonathan. "Pathophysiology of sepsis: role of nitric oxide and other mediators." Current Opinion in Anaesthesiology 8, no. 2 (April 1995): 109–13. http://dx.doi.org/10.1097/00001503-199504000-00002.

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22

Karaca, Semsettin, Mustafa Kulac, Efkan Uz, Irfan Barutcu, and H. Ramazan Yilmaz. "Is nitric oxide involved in the pathophysiology of essential hyperhidrosis?" International Journal of Dermatology 46, no. 10 (October 2007): 1027–30. http://dx.doi.org/10.1111/j.1365-4632.2007.03243.x.

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23

Schulze-Neick, Ingram, and Andrew N. Redington. "Sildenafil, Nitric Oxide, and Acute Lung Injury: Pathophysiology Beats Pharmacotherapy?" Pediatric Research 55, no. 3 (March 2004): 370–71. http://dx.doi.org/10.1203/01.pdr.0000112096.46811.be.

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24

Tidball, James G., and Michelle Wehling-Henricks. "Nitric oxide synthase deficiency and the pathophysiology of muscular dystrophy." Journal of Physiology 592, no. 21 (October 9, 2014): 4627–38. http://dx.doi.org/10.1113/jphysiol.2014.274878.

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25

Münzel, T., T. Heitzer, and D. G. Harrison. "The physiology and pathophysiology of the nitric oxide/superoxide system." Herz 22, no. 3 (June 1997): 158–72. http://dx.doi.org/10.1007/bf03044353.

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26

Petit, Priscilla C., David H. Fine, Gregory B. Vásquez, Lucas Gamero, Mark S. Slaughter, and Kurt A. Dasse. "The Pathophysiology of Nitrogen Dioxide During Inhaled Nitric Oxide Therapy." ASAIO Journal 63, no. 1 (2017): 7–13. http://dx.doi.org/10.1097/mat.0000000000000425.

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27

Noris, Marina, and Giuseppe Remuzzi. "Physiology and Pathophysiology of Nitric Oxide in Chronic Renal Disease." Proceedings of the Association of American Physicians 111, no. 6 (November 15, 1999): 602–10. http://dx.doi.org/10.1046/j.1525-1381.1999.99256.x.

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28

Moncada, Salvador. "P/17 Nitric oxide: Mitochondrial interactions in physiology and pathophysiology." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1777 (July 2008): S6. http://dx.doi.org/10.1016/j.bbabio.2008.05.029.

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29

Styles, Lori. "Nitric Oxide Effects in Sickle Cell Disease." Blood 112, no. 11 (November 16, 2008): sci—48—sci—48. http://dx.doi.org/10.1182/blood.v112.11.sci-48.sci-48.

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Sickle cell disease (SCD) is a complex hemoglobinopathy characterized by microvascular occlusion and hemolytic anemia. Patients suffer from a myriad of both acute and chronic problems affecting virtually every organ system. Historically, microvascular occlusion has been the focus of scientific investigations into these manifestations and the chronic hemolysis of SCD was overlooked. More recently, however, the importance of the pathophysiology of hemolysis has been appreciated and related to a subset of the clinical manifestations of SCD, including pulmonary hypertension, priapism, skin ulcers,

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30

Hamad, Ahmed M., Andrew Clayton, Baharul Islam, and Alan J. Knox. "Guanylyl cyclases, nitric oxide, natriuretic peptides, and airway smooth muscle function." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 5 (November 2003): L973—L983. http://dx.doi.org/10.1152/ajplung.00033.2003.

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Airway smooth muscle (ASM) plays an important role in asthma pathophysiology through its contractile and proliferative functions. The cyclic nucleotides adenosine 3′,5′-cyclic monophosphate (cAMP) and guanosine 3′,5′-cyclic monophosphate (cGMP) are second messengers capable of mediating the effects of a variety of drugs and hormones. There is a large body of evidence to support the hypothesis that cAMP is a mediator of the ASM's relaxant effects of drugs, such as β2-adrenoceptor agonists, in human airways. Although most attention has been paid to this second messenger and the signal transducti

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31

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 q

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32

Udayakumar, Rathna, and Anita Muthupandian. "Role of nitric oxide in the pathophysiology of pregnancy-induced hypertension." International Journal of Medical Science and Public Health 7, no. 11 (2019): 1. http://dx.doi.org/10.5455/ijmsph.2019.0926002102018.

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33

Ahanchi, Sadaf S., Nick D. Tsihlis, and Melina R. Kibbe. "The role of nitric oxide in the pathophysiology of intimal hyperplasia." Journal of Vascular Surgery 45, no. 6 (June 2007): A64—A73. http://dx.doi.org/10.1016/j.jvs.2007.02.027.

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34

R. Swaroop, P.A.T. Kelly, H. S. Bel, G. "The effects of chronic nitric oxide synthase suppression on glioma pathophysiology." British Journal of Neurosurgery 14, no. 6 (January 2000): 543–48. http://dx.doi.org/10.1080/02688690020005554.

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35

Scatena, Roberto, Patrizia Bottoni, Giuseppe E. Martorana, and Bruno Giardina. "Nitric oxide donor drugs: an update on pathophysiology and therapeutic potential." Expert Opinion on Investigational Drugs 14, no. 7 (July 2005): 835–46. http://dx.doi.org/10.1517/13543784.14.7.835.

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36

Kashiwagi, Maki, Roland Zimmermann, and Ernst Beinder. "Pathophysiology of pre-eclampsia: Update on the role of nitric oxide." Current Hypertension Reports 5, no. 6 (December 2003): 493–97. http://dx.doi.org/10.1007/s11906-003-0057-2.

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37

Tummanapalli, Shyam Sunder, Rajesh Kuppusamy, Jia Hao Yeo, Naresh Kumar, Elizabeth J. New, and Mark D. P. Willcox. "The role of nitric oxide in ocular surface physiology and pathophysiology." Ocular Surface 21 (July 2021): 37–51. http://dx.doi.org/10.1016/j.jtos.2021.04.007.

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38

Gawrys, Jakub, Damian Gajecki, Ewa Szahidewicz-Krupska, and Adrian Doroszko. "Intraplatelet L-Arginine-Nitric Oxide Metabolic Pathway: From Discovery to Clinical Implications in Prevention and Treatment of Cardiovascular Disorders." Oxidative Medicine and Cellular Longevity 2020 (March 4, 2020): 1–11. http://dx.doi.org/10.1155/2020/1015908.

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Despite the development of new drugs and other therapeutic strategies, cardiovascular disease (CVD) remains still the major cause of morbidity and mortality in the world population. A lot of research, performed mostly in the last three decades, revealed an important correlation between “classical” demographic and biochemical risk factors for CVD, (i.e., hypercholesterolemia, hyperhomocysteinemia, smoking, renal failure, aging, diabetes, and hypertension) with endothelial dysfunction associated directly with the nitric oxide deficiency. The discovery of nitric oxide and its recognition as an en

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39

Gokce, Aylin Hande, Feridun Suat Gokce, Sinem Durmus, Ramila Hajiyeva, Feyzullah Ersoz, Remise Gelisgen, and Hafize Uzun. "The effect of nitric oxide, endothelial nitric oxide synthetase, and asymmetric dimethylarginine in hemorrhoidal disease." Revista da Associação Médica Brasileira 66, no. 8 (August 2020): 1128–33. http://dx.doi.org/10.1590/1806-9282.66.8.1128.

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SUMMARY AIM The aim of this study was to examine the roles of nitric oxide (NOx), endothelial nitric oxide synthetase (eNOS), and asymmetric dimethylarginine (ADMA), which is the major endogenous inhibitor of nitric oxide synthases (NOS), in the pathophysiology of hemorrhoidal disease. METHODS This study included 54 patients with grades 3 and 4 internal hemorrhoidal disease and 54 patients without the disease who attended the General Surgery Clinic. NOx, eNOS, and ADMA levels were measured with the Enzyme-Linked ImmunoSorbent Assay (ELISA) method. RESULTS The patients had higher NO and eNOS le

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40

Grisham, Matthew B., and Satoshi Aiko. "Nitric oxide and chronic colitis." Canadian Journal of Gastroenterology 10, no. 3 (1996): 199–202. http://dx.doi.org/10.1155/1996/673681.

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Nitric oxide (NO) is thought to play an important role in modulating the inflammatory response by virtue of its ability to affect bloodflow, leukocyte function and cell viability. The objective of this study was to assess the role that NO may play in mediating the mucosal injury and inflammation in a model of chronic granulomatous colitis using two pharmacologically different inhibitors of nitric oxide synthase (NOS). Chronic granulomatous colitis with liver and spleen inflammation was induced in female Lewis rats via the subserosal (intramural) injection of peptidoglycan/polysaccharide (PG/PS

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41

Barnes, Theresa J., Maxwell A. Hockstein, and Craig S. Jabaley. "Vasoplegia after cardiopulmonary bypass: A narrative review of pathophysiology and emerging targeted therapies." SAGE Open Medicine 8 (January 2020): 205031212093546. http://dx.doi.org/10.1177/2050312120935466.

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Cardiovascular disease remains the leading cause of death in the United States, and cardiopulmonary bypass is a cornerstone in the surgical management of many related disease states. Pathophysiologic changes associated both with extracorporeal circulation and shock can beget a syndrome of low systemic vascular resistance paired with relatively preserved cardiac output, termed vasoplegia. While increased vasopressor requirements accompany vasoplegia, related pathophysiologic mechanisms may also lead to true catecholamine resistance, which is associated with further heightened mortality. The int

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42

Le Cras, Timothy D., and Ivan F. McMurtry. "Nitric oxide production in the hypoxic lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (April 1, 2001): L575—L582. http://dx.doi.org/10.1152/ajplung.2001.280.4.l575.

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Nitric oxide (NO) is a potent vasodilator and inhibitor of vascular remodeling. Reduced NO production has been implicated in the pathophysiology of pulmonary hypertension, with endothelial NO synthase (NOS) knockout mice showing an increased risk for pulmonary hypertension. Because molecular oxygen (O2) is an essential substrate for NO synthesis by the NOSs and biochemical studies using purified NOS isoforms have estimated the Michaelis-Menten constant values for O2 to be in the physiological range, it has been suggested that O2substrate limitation may limit NO production in various pathophysi

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43

Medina, Alejandro Marín, Eduardo Esteban Zubero, Moisés Alejandro Alatorre Jiménez, Sara Anabel Alonso Barragan, Carlos Arturo López García, José Juan Gómez Ramos, Juan Francisco Santoscoy Gutierrez, and Zurisadai González Castillo. "NOS3 Polymorphisms and Chronic Kidney Disease." Brazilian Journal of Nephrology 40, no. 3 (May 28, 2018): 273–77. http://dx.doi.org/10.1590/2175-8239-jbn-3824.

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ABSTRACT Chronic kidney disease (CKD) is a multifactorial pathophysiologic irreversible process that often leads to a terminal state in which the patient requires renal replacement therapy. Most cases of CKD are due to chronic-degenerative diseases and endothelial dysfunction is one of the factors that contribute to its pathophysiology. One of the most important mechanisms for proper functioning of the endothelium is the regulation of the synthesis of nitric oxide. This compound is synthesized by the enzyme nitric oxide synthase, which has 3 isoforms. Polymorphisms in the NOS3 gene have been i

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44

Terpolilli, Nicole A., Michael A. Moskowitz, and Nikolaus Plesnila. "Nitric Oxide: Considerations for the Treatment of Ischemic Stroke." Journal of Cerebral Blood Flow & Metabolism 32, no. 7 (February 15, 2012): 1332–46. http://dx.doi.org/10.1038/jcbfm.2012.12.

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Some 40 years ago it was recognized by Furchgott and colleagues that the endothelium releases a vasodilator, endothelium-derived relaxing factor (EDRF). Later on, several groups identified EDRF to be a gas, nitric oxide (NO). Since then, NO was identified as one of the most versatile and unique molecules in animal and human biology. Nitric oxide mediates a plethora of physiological functions, for example, maintenance of vascular tone and inflammation. Apart from these physiological functions, NO is also involved in the pathophysiology of various disorders, specifically those in which regulatio

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45

Fidan, Işıl, Sevgi Yüksel, Turgut Ýmir, Ceyla İrkeç, and F. Nur Aksakal. "The importance of cytokines, chemokines and nitric oxide in pathophysiology of migraine." Journal of Neuroimmunology 171, no. 1-2 (February 2006): 184–88. http://dx.doi.org/10.1016/j.jneuroim.2005.10.005.

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46

Rosselli, M. "Role of nitric oxide in the biology, physiology and pathophysiology of reproduction." Human Reproduction Update 4, no. 1 (January 1, 1998): 3–24. http://dx.doi.org/10.1093/humupd/4.1.3.

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Bivalacqua, T. J., H. C. Champion, and W. J. G. Hellstrom. "Implications of nitric oxide synthase isoforms in the pathophysiology of Peyronie's disease." International Journal of Impotence Research 14, no. 5 (October 2002): 345–52. http://dx.doi.org/10.1038/sj.ijir.3900872.

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Gossmann, Jan, Androniki Radounikli, Alexander Bernemann, Oliver Schellinski, Hans-Peter Raab, Ralf Bickeböller, and Ernst-Heinrich Scheuermann. "Pathophysiology of Cyclosporine-Induced Nephrotoxicity in Humans: A Role for Nitric Oxide?" Kidney and Blood Pressure Research 24, no. 2 (2001): 111–15. http://dx.doi.org/10.1159/000054216.

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Tripathy, D., J. Chakraborty, and K. P. Mohanakumar. "Antagonistic pleiotropic effects of nitric oxide in the pathophysiology of Parkinson's disease." Free Radical Research 49, no. 9 (June 4, 2015): 1129–39. http://dx.doi.org/10.3109/10715762.2015.1045505.

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Zhang, Yin Hua, Chun Zi Jin, Ji Hyun Jang, and Yue Wang. "Molecular mechanisms of neuronal nitric oxide synthase in cardiac function and pathophysiology." Journal of Physiology 592, no. 15 (May 27, 2014): 3189–200. http://dx.doi.org/10.1113/jphysiol.2013.270306.

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