Статті в журналах: "Nitric oxide Pathophysiology"

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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6

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 to prevent nitric oxide-associated tissue injury. Compounds that release nitric oxide in small amounts over a prolonged period of time may also be very useful for prevention of gastrointestinal injury associated with shock and with the use of drugs that have ulcerogenic effects. Indeed, the coupling of a nitric oxide-releasing moiety to nonsteroidal anti-inflammatory drugs has proven to be a valid means of substantially reducing the gastrointestinal toxicity of these drugs without decreasing their efficacy.

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 also results in decreased NOS activities in the placental villi, suggesting that problems attributed to smoking during pregnancy could be linked to NO metabolism. Polyamines arginine and citrulline (all of which are important metabolites in the NO pathway) were also measured in placental villous tissues. The data presented in this review article are from work carried out in the authors' laboratories and suggest that alterations in the placental arginine-NO pathway may not only play a role in the physiological changes of advancing gestation but may also contribute to the pathophysiology of pre-eclampsia and fetal growth retardation.

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 cluster headache patients (n = 542) and controls (n = 581) were genotyped using TaqMan® assays on an Applied Biosystems 7500 qPCR cycler. This is the largest performed genetic study on NOS involvement in cluster headache so far. We found an association between cluster headache and one iNOS haplotype consisting of the minor alleles of rs2297518 and rs2779249 (p = 0.022). In addition, one of the analyzed nNOS variants, rs2682826, was associated with reported triptan use (p = 0.039). Our data suggest that genetic variants in NOS genes do not have a strong influence on cluster headache pathophysiology, but that certain combinations of genetic variants in NOS genes may influence the risk of developing the disorder or triptan use.

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, and possibly stroke. This subphenotype of SCD has been convincingly related to impaired nitric oxide (NO) homeostasis due to hemolysis. NO has pleiotropic effects including vaso-dilatory, antioxidative, anti-adhesion, and anti-thrombotic properties, which are all potentially important in the pathophysiology of SCD. Perturbation of NO homeostasis, therefore, could profoundly impact patients with SCD. Animal and human data support a state of “NO resistance” in SCD patients. Human studies have shown that SCD patients have a decreased response to exogenous NO donors and that is likely due to the scavenging of NO by free plasma hemoglobin that results from ongoing hemolysis. “NO resistance” is further augmented by the increased levels of reactive oxygen species (ROS) known to occur in SCD patients. High levels of ROS favor additional hemolysis through increased oxidant stress on the sickle red blood cell and reduce NO bioavailability by inactivation of circulating NO. With the substantial human and animal data to support a role for “NO resistance” in the pathophysiology of SCD, investigation with NO-based therapy have begun. Several approaches to overcoming “NO resistance” can be devised including increasing the precursors to NO, decreasing hemolysis, direct NO donors, and decreasing oxidant stress. To date, studies evaluating arginine (NO precursor), inhaled NO, and sildenafil (NO donor) have been reported. Oral arginine showed no benefit in a large clinical trial, and a preliminary trial of inhaled NO had only minimal benefit. Sildenafil may be more promising and is under further study. Lastly, although impaired NO bioavailability has been related to a subset of patients with pulmonary hypertension, skin ulcers and priapism, it will be important to determine what impact NO has on other manifestations, such as vaso-occlusive pain episodes and whether NO modulation can also be used therapeutically in this setting.

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 transduction pathways it activates, recent evidence suggests that cGMP is also an important second messenger in ASM with important relaxant and antiproliferative effects. Here, we review the regulation and function of cGMP in ASM and discuss the implications for asthma pathophysiology and therapeutics. Recent studies suggest that activators of soluble and particulate guanylyl cyclases, such as nitric oxide donors and natriuretic peptides, have both relaxant and antiproliferative effects that are mediated through cGMP-dependent and cGMP-independent pathways. Abnormalities in these pathways may contribute to asthma pathophysiology, and therapeutic manipulation may complement the effects of β2-adrenoceptor agonists.

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 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.

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 endothelial-derived relaxing factor was a breakthrough in understanding the pathophysiology and development of cardiovascular system disorders. The nitric oxide synthesis pathway and its regulation and association with cardiovascular risk factors were a common subject for research during the last decades. As nitric oxide synthase, especially its endothelial isoform, which plays a crucial role in the regulation of NO bioavailability, inhibiting its function results in the increase in the cardiovascular risk pattern. Among agents altering the production of nitric oxide, asymmetric dimethylarginine—the competitive inhibitor of NOS—appears to be the most important. In this review paper, we summarize the role of L-arginine-nitric oxide pathway in cardiovascular disorders with the focus on intraplatelet metabolism.

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 levels and lower ADMA levels than the control subjects (p<0.001). A significant highly positive correlation was found between NO and eNOS (p<0.001). Nevertheless, there was a highly negative correlation between ADMA and NO-eNOS(p<0.001, p<0.001). CONCLUSION This preliminary study reveals that higher NOx and eNOS activities and lower ADMA levels in the rectal mucosa are observed in patients with hemorrhoidal disease than in those with normal rectal tissue. The imbalance between endothelium-derived relaxing factors, such as NO and endogenous competitive inhibitor of NOS, ADMA, may cause hemorrhoidal disease. Our study proposes that hemorrhoids display apparent vascular dilatation and present with bleeding or swelling. ADMA is an effective NOS inhibitor and may be a promising therapeutic option for hemorrhoidal disease.

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) derived from group A streptococci. Chronic NOS inhibition by oral administration of NG-nitro-L-arginine methyl ester (L-NAME) (15 µmol/kg/day) or amino-guanidine (AG) (15 µmol/ kg/day) was found to attenuate the PG/PS-induced increases in macroscopic colonic inflammation scores and colonic myeloperoxidase activity. Only AG -- not L-NAME – attenuated the PG/PS-induced increases in colon dry weight. Both L-NAME and AG significantly attenuated the PG/PS-induced increases in spleen weight whereas neither was effective at significantly attenuating the PG/PS-induced increases in liver weight. Although both L-NAME and AG inhibited NO production in vivo, as measured by decreases in plasma nitrite and nitrate levels, only AG produced significantly lower values (38±3 versus 83±8 µM, respectively, P<0.05). Finally, L-NAME, but not AG, administration significantly increased mean arterial pressure from 83 mmHg in colitic animals to 105 mmHg in the PG/PS+ L-NAME-treated animals (P<0.05). It is concluded that NO may play an important role in mediating some of the pathophysiology associated with this model of chronic granulomatous colitis.

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 introduction of a second non-catecholamine vasopressor, angiotensin II, and non-specific nitric oxide scavengers offers potential means by which to manage this challenging phenomenon. This narrative review addresses both the definition, risk factors, and pathophysiology of vasoplegia and potential therapeutic interventions.

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 pathophysiological conditions including hypoxia. This review summarizes numerous studies of the effects of acute and chronic hypoxia on NO production in the lungs of humans and animals as well as in cultured vascular cells. In addition, the effects of hypoxia on NOS expression and posttranslational regulation of NOS activity by other proteins are also discussed. Most studies found that hypoxia limits NO synthesis even when NOS expression is increased.

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 implicated as factors that alter the homeostasis of this mechanism. The Glu298Asp polymorphisms 4 b/a and -786T>C of the NOS3 gene have been associated with a more rapid deterioration of kidney function in patients with CKD. These polymorphisms have been evaluated in patients with CKD of determined and undetermined etiology and related to a more rapid deterioration of kidney function.

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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 regulation of blood flow and inflammation has a key role. The aim of the current review is to summarize the role of NO in cerebral ischemia, the most common cause of stroke.

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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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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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