Relevant bibliographies by topics / Thromboxane synthase inhibitors

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Thromboxane synthase inhibitors'

Author: Grafiati
Published: 5 June 2025
Last updated: 2 August 2025

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Journal articles on the topic "Thromboxane synthase inhibitors"

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Chen, Liying, Mina N. Salafranca, and Jawahar L. Mehta. "Cyclooxygenase inhibition decreases nitric oxide synthase activity in human platelets." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 4 (1997): H1854—H1859. http://dx.doi.org/10.1152/ajpheart.1997.273.4.h1854.

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Activity of both nitric oxide (NO) synthase (NOS) and cyclooxygenase (COX) plays an important role in the regulation of platelet function. NO has been shown to directly activate COX. This study was designed to determine whether products of the COX pathway in turn regulate NOS activity. Human platelets were incubated with aspirin, indomethacin, the selective thromboxane A2 synthase inhibitor U-63557A, or the prostaglandin H2-thromboxane A2-receptor blocker SQ-29548 for 1 h at 37°C. Multiple indexes of the activity of thel-arginine-NO pathway and changes in cytosolic Ca2+concentration ([Ca2+]i)
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Carter, A. J., and S. Heptinstall. "Platelet Aggregation in Whole Blood: The Role of Thromboxane A2 and Adenosine Diphosphate." Thrombosis and Haemostasis 54, no. 03 (1985): 612–16. http://dx.doi.org/10.1055/s-0038-1660081.

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SummaryThe platelet aggregation that occurred in whole blood in response to several aggregating agents (collagen, arachidonic acid, adenosine diphosphate, adrenaline and thrombin) was measured using an Ultra-Flo 100 Whole Blood Platelet Counter. The amounts of thromboxane B2 produced were measured by radioimmunoassay. The effects of various inhibitors of thromboxane synthesis and the effects of apyrase, an enzyme that destroys adenosine diphosphate, were determined.Platelet aggregation was always accompanied by the production of thromboxane B2, and the amounts produced depended on the nature a
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Mangino, M. J., and C. C. Chou. "Thromboxane synthesis inhibitors and postprandial jejunal capillary exchange capacity." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 5 (1988): G695—G701. http://dx.doi.org/10.1152/ajpgi.1988.254.5.g695.

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The effects of thromboxane synthesis inhibitors (imidazole and U 63557A; Upjohn) and the cyclooxygenase inhibitor, mefenamic acid, on jejunal capillary filtration coefficients (Kfc) were determined in dogs before and during the presence of predigested food in the jejunal lumen. The jejunal Kfc increased significantly soon after the placement of a predigested test food containing all major constituents of diet. The Kfc remained elevated as long as the food was present in the lumen (15 min). Mefenamic acid (10 mg/kg iv) did not significantly alter resting jejunal Kfc or alter the food-induced in
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Vermylen, Jos, and Hans Deckmyn. "Thromboxane synthase inhibitors and receptor antagonists." Cardiovascular Drugs and Therapy 6, no. 1 (1992): 29–33. http://dx.doi.org/10.1007/bf00050914.

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Ksander, Gary M., Mark Erion, Andrew M. Yuan, et al. "Dual Angiotensin Converting Enzyme/Thromboxane Synthase Inhibitors." Journal of Medicinal Chemistry 37, no. 12 (1994): 1823–32. http://dx.doi.org/10.1021/jm00038a011.

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Shi, H., A. Yokoyama, N. Kohno, et al. "Effect of thromboxane A2 inhibitors on allergic pulmonary inflammation in mice." European Respiratory Journal 11, no. 3 (1998): 624–29. http://dx.doi.org/10.1183/09031936.98.11030624.

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Thromboxane (Tx)A2 synthase inhibitors and thromboxane prostanoid (TP) receptor antagonists have been developed as anti-asthma drugs. TxA2 may contribute to airflow limitation and bronchial hyperresponsiveness, and these compounds have been demonstrated to improve them. However, it is not known whether TxA2 is involved in bronchial inflammation. To address this question, we explored the influences of OKY-046 (a TxA2 synthase inhibitor) and S-1452 (a TP receptor antagonist) on eosinophilic inflammation of the airways using a murine model. BALB/c mice sensitized with ovalbumin and challenged by
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Farrukh, I. S., J. R. Michael, W. R. Summer, N. F. Adkinson, and G. H. Gurtner. "Thromboxane-induced pulmonary vasoconstriction: involvement of calcium." Journal of Applied Physiology 58, no. 1 (1985): 34–44. http://dx.doi.org/10.1152/jappl.1985.58.1.34.

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Infusion of tert-butyl hydroperoxide (t-bu-OOH) or arachidonic acid into rabbit pulmonary arteries stimulated thromboxane B2 (TxB2) production and caused pulmonary vasoconstriction. Both phenomena were blocked by cyclooxygenase inhibitors or a thromboxane synthase inhibitor. The increase in pulmonary arterial pressure caused by either t-bu-OOH or arachidonic acid infusion correlated with the concentration of TxB2 in the effluent perfusate. The concentration of TxB2 in the effluent perfusate, however, was always 10-fold greater after arachidonic acid infusion. In the rabbit pulmonary vascular b
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Cimetière, Bernard, Thierry Dubuffet, Caroline Landras, et al. "New tetrahydronaphthalene derivatives as combined thromboxane receptor antagonists and thromboxane synthase inhibitors." Bioorganic & Medicinal Chemistry Letters 8, no. 11 (1998): 1381–86. http://dx.doi.org/10.1016/s0960-894x(98)00221-2.

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Gresele, Paolo, Hans Deckmyn, Giuseppe G. Nenci, and Jos Vermylen. "Thromboxane synthase inhibitors, thromboxane receptor antagonists and dual blockers in thrombotic disorders." Trends in Pharmacological Sciences 12 (January 1991): 158–63. http://dx.doi.org/10.1016/0165-6147(91)90533-x.

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Ackerley, Norman, Andrew G. Brewster, George R. Brown, et al. "A Novel Approach to Dual-Acting Thromboxane Receptor Antagonist/Synthase Inhibitors Based on the Link of 1,3-Dioxane-Thromboxane Receptor Antagonists and -Thromboxane Synthase Inhibitors." Journal of Medicinal Chemistry 38, no. 10 (1995): 1608–28. http://dx.doi.org/10.1021/jm00010a005.

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Dissertations / Theses on the topic "Thromboxane synthase inhibitors"

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Hatziantoniou, Christos. "Utilisation des inhibiteurs sélectifs de la thromboxane-synthétase rénale chez le rat : effets sur le développement de l'insuffisance rénale aiguë induite par le glycérol, effets sur l'excrétion sodique." Paris 11, 1987. http://www.theses.fr/1987PA112010.

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Le rôle du thromboxane A2 rénal sur le développement de l'insuffisance rénale aiguë induite par le glycérol et sur l'excrétion sodique, a été étudié chez le rat en utilisant des inhibiteurs sélectifs de sa synthèse. Les constatations principales de ce travail sont les suivantes :a)le thromboxane A2 glomérulaire est un des agents qui participent à l'installation de l'insuffisance rénale aiguë induite par le glycérol, et b) le thromboxane A2 exerce une action anti-natriurétique qui devient importante dans des cas pathologiques accompagnés par une activation du thromboxane rénal<br>The effects of
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"Suppression of thromboxane synthase inhibits lung cancer cell proliferation." Thesis, 2008. http://library.cuhk.edu.hk/record=b6074592.

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Further studies were done to investigate the mechanism responsible for 1-BI-induced apoptosis in NCI-H460. It was found that 1-BI stimulated the expression of pro-apoptotic p53, Bax and cytosolic NF-kB p65 subunit but decreased pERK in NCI-H460 cells. The active forms of caspase 3 and caspase 9 were detected by Western blot, accompanied by an increase in caspase 3 activity. Reactive oxygen species (ROS) was highly generated at 24 hours after the treatment and the mitochondrial membrane potential was significantly decreased at 48 and 72 hours. The application of either N-acetyl cysteine (NAC) o
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Yu, Hsiao-Ying, and 俞曉頴. "To Evaluate the Effects of Thromboxane A2 Synthase Inhibitor on the Bone mass of Senile mouse." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/99209356530412370441.

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碩士<br>中原大學<br>生物科技研究所<br>101<br>Osteoporosis is an important health issue in postmenopausal women and elderly persons. Although there are no obvious clinical symptoms, minor trauma may cause fractures and other related complications which may severely impact on patients' life quality and life span. Ghosal hematodiaphyseal dysplasia syndrome (GHDD) is a disorder with higher bone density. Genetic studies of patients with this disorder had identified mutations in the gene encoding thromboxane A2 synthase (TXAS), which is the key enzyme for producing thromboxane A2 (TXA2). TXA2 was indicated to be
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Vogel, York Christoph. "Wirkungen einer kombinierten Hemmung der Thromboxan-Synthase und der Thromboxan-Rezeptoren durch den äquipotenten Inhibitor Terbogrel bei Ischämie und Reperfusion am Schweineherzen /." 2004. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=013193439&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Books on the topic "Thromboxane synthase inhibitors"

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Peterka, Andrea Maria-Luise. Tierexperimentelle Untersuchung über den Einfluss des Thromboxan-Synthese-Inhibitors Imidazol auf die Minderdurchblutung der partiell gestauten Niere. 1986.

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Book chapters on the topic "Thromboxane synthase inhibitors"

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Davì, Giovanni, Francesca Santilli, and Natale Vazzana. "Thromboxane Receptors Antagonists and/or Synthase Inhibitors." In Antiplatelet Agents. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-29423-5_11.

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Patrono, Carlo, Paola Filabozzi, and Paola Patrignani. "The Effects of Low-Dose Aspirin and Selective Inhibitors of Thromboxane-Synthase on Eicosanoid Production in Man." In Drugs Affecting Leukotrienes and Other Eicosanoid Pathways. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-7841-9_11.

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Yoshida, Tadashi, Hideto Kameda, Akizuki Masashi, Mitsuo Homma, and Yasuo Ikeda. "Improvement of Renal Function with Selective Thromboxane A2 Synthetase Inhibitor, DP-1904 in Lupus Nephritis." In Advances in Experimental Medicine and Biology. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1810-9_23.

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Doig, M. V., and R. A. Clare. "Developing Methods for a Thromboxane Synthetase Inhibitor and a Prostacyclin Analogue in Biological Fluids: Problems and Some Solutions." In Bioanalysis of Drugs and Metabolites, Especially Anti-Inflammatory and Cardiovascular. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-9424-3_7.

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COLLINGTON, E., and H. FINCH. "Chapter 11 Thromboxane Synthase Inhibitors and Receptor Antagonists." In Annual Reports in Medicinal Chemistry. Elsevier, 1990. http://dx.doi.org/10.1016/s0065-7743(08)60015-9.

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Collington, Eric W., and Harry Finch. "Chapter 11. Thromboxane Synthase Inhibitors and Receptor Antagonists." In Annual Reports in Medicinal Chemistry. Elsevier, 1990. http://dx.doi.org/10.1016/s0065-7743(08)61587-0.

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Cross, Peter E., and Roger P. Dickinson. "Chapter 10 Thromboxane Synthetase Inhibitors and Antagonists." In Annual Reports in Medicinal Chemistry. Elsevier, 1987. http://dx.doi.org/10.1016/s0065-7743(08)61158-6.

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Conference papers on the topic "Thromboxane synthase inhibitors"

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De Clerck, F., R. Van de Wiele, B. Xhonneux, et al. "PLATELET TXA2 SYNTHETASE INHIBITION AND TXA2/PROSTAGLANDIN ENDOPEROXIDE RECEPTOR BLOCKADE COMBINED IN ONE MOLECULE (R 68070)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643465.

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F 68070, an oxime-alkane carboxylic acid derivative (Janssen Pharmaceutica), is a potent inhibitor of thromboxane A2 (TXA2) synthetase activity (IC50 in vitro against thrombin-stimulated human platelets in plasma : R 68070 : 2.9 x 10-8 M; CGS 13080 : 6 x 10-8 M; OKY-1581 : 8.2 x 10-8 M; dazmegrel : 2.6 x 10-8 M; dazoxiben : 2.3 x 10-8 M).The compound specifically inhibits platelet TXA2 synthetase activity (14C-arachidonic acid metabolism by washed human platelets) without effect on the cyclo-oxygenase, lipoxygenase (platelets, RBL cells) or prostacyclin synthetase activities (rat aortic rings)
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Saldeen, P., and T. Saldeen. "THROMBOXANE PRODUCTION BY PATHOLOGICAL VESSELS AND ITS POSSIBLE CONTRIBUTIION TO THE DEVELOPMENT OF THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643380.

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It has been proposed that a decreased synthesis of PGI2 may be a critical factor in the development of thrombosis on the basis that generation of PGI2 may under ly the ability of normal vessels to resist platelet adhesion. Vascular synthesis of thromboxane A2 (Tx) has been believed to be nonexistent or of very slight degree and of no physiological or pathological importance. Recent studies, however, have shown that other soirees of Tx than platelets may exist. Veins from patients with deep venous thrombosis, atheromatous arteries from patients, autopsy cases and rabbits with atheromatosis, and
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Lumley, P., E. W. Collington, P. Hallett, et al. "THE EFFECTS OF GR32191, A NEW THROMBOXANE RECEPTOR BLOCKING DRUG,ON PLATELETS AND VASCULAR SMOOTH MUSCLE IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643754.

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The effect of a new thromboxane receptor blocking drug GR32191 ([1R-[1α(Z),2β,3β,5α]]-(+)-7-[5-[[(1,1"-biphenyl)-4-yl]methoxy] -3-hydroxy-2-(l-piperidinyl)cyclopentyl]-4-heptenoic acid,hydrochloride) has been examined upon platelets and vascular smooth muscle. In human platelet-rich plasma (PRP), aggregation to thromboxane(Tx) A2, PGH2, arachidonic acid, collagen andU-46619 was antagonised by GR32191 (IC50 range 2-36 nM).Primary aggregation (PRP treated with aspirin 10 pM) to ADP, 5-HT and adrenaline were unaffected by concentrations of GR32191 up to 10 pM. In human PRP, U-46619-induced aggreg
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Sheehan, S. J., A. B. Latif, S. R. Bibby, R. C. Kester, and S. M. Rajah. "THE RECOVERY OF ENDOTHELIAL CELL AND PLATELET PROSTAGLANDIN SYNTHESES AFTER ADMINISTRATION OF ASPIRIN AND INDOBUFEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643389.

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Suppression of endothelial prostacyclin (PGI2) by cyclooxygenase inhibition may contribute to the formation of neointimal hyperplasia. While aspirin (ASA) inhibits platelet function for several days, it returns to normal within 24 hours after indobufen (IDB), a reversible cyclooxygenase inhibitor, suggesting that prostacyclin may recover at an even faster rate. In a randomised, controlled study, recovery of platelet and endothelial cell prostaglandin synthesis was compared in 49 New Zealand white rabbits following indobufen (3.5 mg/kg) or aspirin (5 mg/kg). Prostacyclin in arterial incubates a
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Norϕ, A., T. Smimonsen, K. Ytre-Arene, B. Lyngmo, and B. Svensson. "THE EFFECT OF TWO CHOLESTEROL-LOWERING AGENTS ON PLATELETS IN PATIENTS WITH HYPERCHOLESTEROLEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643801.

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Twenty-one subjects with type Ila hyperlipoproteinemia, receiving dietary treatment were given Synvinolin (MK-733), a HMG-CoA reductase inhibitor, 40 mg or Cholestyramin (Questran) 24 g daily for a period of 12 weeks.Serum lipids, platelet cholesterol, phospholipids and fatty acid composition and platelet function were measured before and after the intake of the two drugs.Both drugs reduced serum total cholesterol with approximately 50%. No significant changes were observed in platelet lipid concentrations or in the primary bleeding time. Collagen induced aggregation and thromboxane (TXA2) pro
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Patscheke, H., K. Stegmeier, W. Hornberger, Ch Staiger, and G. Neugebauer. "INHIBITION OF PLATELET ACTIVATION BY THE NOVEL THROMBOXANE RECEPTOR ANTAGONIST BM 13.505." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643469.

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The effects of BM 13.505 (4-[2-(4-Chlorobenzenesulfonylami-no)ethyl]-benzene acetic acid = BM) on human washed platelets and platelet-rich plasma (PRP) were studied in vitro and after oral application in 10 male volunteers ex vivo/in vitro. BM inhibited the shape change, aggregation and (1H)serotonin release when the platelets were activated by agents that stimulate via the thromboxane Az/prostaglandin H2 (TXA2/PGH2) receptor. Such agonists were collagen, methyl mercury chloride (methyl-Hg), arachidonic acid and the PGH2 analogue U 46,619. BM was 9 times more potent an inhibitor than sulotroba
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De Chaffoy de Courcells, D., and F. De Clerck. "THE EFFECT OF A COMBINED TXA2SYNTHETASE AND TXA2/PROSTAGLANDIN ENDOPEROXIDE RECEPTOR BLOCKER(R 68 070)ON THE ACTIVATION OF EXCITATORY RECEPTOR-COUPLEDPHOSPHOLIPASE C IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643758.

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Prostaglandin endoperoxides (PGEND) and thromboxane A2 (TxA2)contribute to the activation of platelets, involving inositol-containing phospholipids as a signal transducing system. A primary step in this signal transduction consists of the activation of phospholipase C, which then yields diacylglycerol and inositol phosphates;diacylglycerol is subsequently phosphorylated to phosphatidic acid (PA). In platelets prelabelled with [32P] orthophosphate,receptor activation is quantitatively reflected by an increased formation of [32P]-PA.Using this assay, the relativeimportance of endogenously genera
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Kuhn, M., T. H. Müller, and W. G. Eisert. "CYCLIC THROMBUS FORMATION IN RABBIT AORTA: A NEW MODEL OF ACUTE ARTERIAL THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643174.

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Existing models of arterial thrombosis either require extensive surgical intervention or are limited by the short period of observation. Therefore we developed a new model in rabbits to monitor cyclic flow reductions (CFR) due to thrombus formation in a partially denuded and stenosed aorta.An electromagnetic flowprobe was positioned proximally to a stenosis of the abdominal aorta in anesthetized New Zealand rabbits after limited denudation of the vessel using a hemostat. The aortic blood flow was spontaneously reduced due to formation of thrombi. It returned to the basal level after gently sha
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Stuart, M. J., J. Wu, C. Ganley, and S. Sunderji. "AMNIOTIC FLUID FROM TERM GESTATION ENHANCES PLATELET PRODUCTION OF VASOCONSTRICTOR THROMBOXANE: POTENTIAL ROLE IN PERSISTENT PULMONARY HYPERTENSION IN THE NEONATE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644273.

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One of the causes of persistent pulmonary hypertension (PPH) in the neonate may involve the interaction of amniotic fluid (AF) and pits, with the release of thromboxane A2 (TXA2) causing an increase in pulmonary vascular tone. To prove or disprove this hypothesis, AF from term (n=6) and from 15 to 17 weeks gestation (n=6) were preincubated for 15 minutes with platelet rich plasma followed by the addition of thrombin or arachidonic acid, and plt. TXB2assessed by radioimmunoassay. AF from early gestation had no significant effect on the production of the potent pulmonary vasoconstrictor metaboli
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Giannessi, D., R. De Caterina, G. Lazzerini, R. Sicari, and P. Gazzetti. "RELATIVE SENSITIVITY OF CARDIAC PROSTACYCLIN AND THROMBOXANE TO INHIBITION BY NON-STEROIDAL ANTIINFLAMMATORY DRUGS IN THE RAT HEART." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643390.

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We have previously shown that the isolated perfused rat Langendorff heart is able to synthesize detectable amounts of thromboxane (TX) A2, as well as prostacyclin (PGI2). Eicosanoid production in this system is increased during post-ischemic reperfusion, reflecting greater availability of substrate and net increase of synthesis. We assessed relative sensitivity of cyclooxygenases synthesizing TX and prostacyclin (probably located in different cell types) to aspirin (0.1, 0.5, 1 g/1), ibuprofen (1, 10, 80, 160, 320 mg/1) and diclofenac (0.01, 0.1, 0.5, 2.5, 5, 10, 25 mg/1), by radioimmunoassays
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