Relevant bibliographies by topics / Thromboxane A2/blood

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

Academic literature on the topic 'Thromboxane A2/blood'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Thromboxane A2/blood"

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Narumiya, Shuh, Fumitaka Ushikubi, Masatoshi Nakajima, Masakazu Hirata, Minoru Okuma, and Motohatsu Fujiwara. "Development of thromboxane A2 antagonists and isolation of thromboxane A2 receptor in human blood platelets." Japanese Journal of Pharmacology 52 (1990): 43. http://dx.doi.org/10.1016/s0021-5198(19)54995-2.

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Hsu, Hsiu-Ching, Ming-Fong Chen, Chii-Ming Lee, and Yuan-Teh Lee. "Determinative Role of Peroxidized Low-Density Lipoprotein in Myocardial Thromboxane Synthesis during Pacing-Induced Ischaemia in Humans." Clinical Science 94, no. 1 (1998): 29–34. http://dx.doi.org/10.1042/cs0940029.

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1. Myocardial thromboxane A2 production increases in patients with pacing-induced ischaemia and correlates with a decrease in myocardial lactate extraction. The release of myocardial thromboxane A2 before any lactate production was observed in patients with unstable angina. This study was proposed to clarify whether the early thromboxane A2 release contributed to the ongoing myocardial ischaemia and to determine which metabolites can be attributed to the thromboxane A2 release. Thirty-five patients with chest pain and positive treadmill exercise test underwent atrial pacing to the predicted ma
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Zoja, C., N. Perico, D. Corna, et al. "Thromboxane synthesis inhibition increases renal prostacyclin and prevents renal disease progression in rats with remnant kidney." Journal of the American Society of Nephrology 1, no. 5 (1990): 799–807. http://dx.doi.org/10.1681/asn.v15799.

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Previous studies have demonstrated that inhibition of thromboxane A2-dependent platelet aggregation by the thromboxane A2 synthase inhibitor, OKY 1581, ameliorated the progressive kidney disease of rats with subtotal renal ablation. OKY 1581 also decreased the excessive renal thromboxane A2 synthesis and lowered systemic blood pressure. In the same model, a low dose aspirin and a specific thromboxane A2 receptor antagonist failed to influence proteinuria, glomerulosclerosis, and hypertension, thus excluding a role for either platelet or renal thromboxane A2 in renal disease progression. The ai
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Wood, C. E., T. A. Cudd, C. Kane, and K. Engelke. "Fetal ACTH and blood pressure responses to thromboxane mimetic U-46619." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 4 (1993): R858—R862. http://dx.doi.org/10.1152/ajpregu.1993.265.4.r858.

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This study was performed to test the hypothesis that thromboxane A2 stimulates increases in fetal adrenocorticotropic hormone (ACTH), vasopressin, or renin secretion and affects fetal cardiovascular function by an action on the fetal central nervous system. We infused a stable synthetic analogue of thromboxane A2, U-46619, into one common carotid artery or inferior vena cava or infused saline into one common carotid artery in chronically catheterized fetal sheep between 127 and 140 days gestation. We found that intracarotid but not intravenous infusions of U-46619 at a rate of 750 ng/min stimu
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Pai, Chen-Hsueh, Shu-Wha Lin, I.-Shing Yu, et al. "Roles of Thromboxane A2 On High Salt Induced-Fetal Defect." Blood 114, no. 22 (2009): 5129. http://dx.doi.org/10.1182/blood.v114.22.5129.5129.

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Abstract Abstract 5129 Introduction Preeclampsia is a pregnancy-induced disorder. If a pregnant woman suffered from preeclampsia, her worse developed-placenta might result in growth retardation of the fetus, and in the most severe cases, it would cause fetal and maternal death. Several previous studies showed that circulating thromboxane A2 in preeclampsic women was higher than that of normal pregnant women, and higher thromboxane A2 level might induce thrombosis and hypertension in these patients. Thus, thromboxane A2 was thought to be an important metabolite relevant to the development of pr
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el Kashef, H. A., and J. D. Catravas. "Prostanoid mediation of pulmonary vascular response to acetylcholine in rabbits." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 4 (1986): H808—H814. http://dx.doi.org/10.1152/ajpheart.1986.251.4.h808.

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We studied the effects of acetylcholine (ACh) in the anesthetized, open-chest rabbit. ACh (5-20 nmol/kg), administered as a bolus into the right jugular vein, produced a dose-dependent increase in both pulmonary arterial pressure and pulmonary vascular resistance but a decrease in systemic arterial pressure and pulmonary blood flow. All these effects were prevented by atropine. Pretreatment with the phospholipase A2 inhibitor quinacrine reduced the pulmonary vascular responses to ACh without affecting systemic arterial pressure. Similarly, treatment with the cyclooxygenase inhibitors indometha
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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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Benyó, Zoltán, Christoph Görlach, and Michael Wahl. "Involvement of Thromboxane A2 in the Mediation of the Contractile Effect Induced by Inhibition of Nitric Oxide Synthesis in Isolated Rat Middle Cerebral Arteries." Journal of Cerebral Blood Flow & Metabolism 18, no. 6 (1998): 616–18. http://dx.doi.org/10.1097/00004647-199806000-00003.

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Inhibition of nitric oxide (NO) synthesis induces vasoconstriction and reduction of the blood flow in the brain, indicating that basal release of NO provides a resting vasore-laxant tone in the cerebral circulation. In the present study, the contractile effect of the NO synthase blocker NG-nitro-L-arginine (100 μmol/L) in isolated rat middle cerebral arteries was attenuated markedly in the presence of the cyclooxygenase inhibitor indomethacin (5 μmol/L), the thromboxane A2 synthase inhibitor ridogrel (10 μmol/L), or the thromboxane receptor antagonist ICI 192605 (100 μmol/L). These results ind
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Eidt, J. F., J. Ashton, P. Golino, J. McNatt, L. M. Buja, and J. T. Willerson. "Thromboxane A2 and serotonin mediate coronary blood flow reductions in unsedated dogs." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 3 (1989): H873—H882. http://dx.doi.org/10.1152/ajpheart.1989.257.3.h873.

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We have shown in anesthetized open-chest dogs that recurrent platelet aggregation at the site of coronary artery stenosis and endothelial injury results in a pattern of cyclical variations in coronary blood flow (CFVs) and that serotonin and thromboxane A2 are important mediators of CFVs. In the present study, we tested the following hypotheses: 1) severe spontaneous reductions in coronary blood flow occur in awake closed-chest dogs with coronary artery stenoses and endothelial injury; 2) there is a progression from CFVs to persistent low coronary blood flow; and 3) serotonin and thromboxane A
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Hirata, Masakazu, Yasunori Hayashi, Fumitaka Ushikubi, et al. "Thromboxane A2 receptor in human blood platelets. 5. Cloning and expression of cDNA for the human thromboxane A2 receptor." Japanese Journal of Pharmacology 55 (1991): 167. http://dx.doi.org/10.1016/s0021-5198(19)38510-5.

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Dissertations / Theses on the topic "Thromboxane A2/blood"

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Schmidt, Renate Luise. "Der Einfluss von Clozapin, N-Desmethylclozapin und Chlorpromazin auf die in-vitro-Produktion von Thromboxan." Doctoral thesis, Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-149801.

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Die Hypothese, dass das AP Clozapin, ebenso wie dessen Metabolit NDMC die Produktion von TxA2 beeinfluss könnten, stellten wir nach ausführlicher Literaturrecherche auf. Letztere zeigte, dass bereits beim ersten AP CPZ eine reduzierende Wirkung auf die TxA2-Produktion nachgewiesen werden konnte. TxA2 und die Aktivierung seines Rezeptors modulieren Vasokonstriktion und Thrombozytenaggregation. Weiterhin nehmen sie Einfluss auf dopaminerge und serotonerge Signalwege. In der Pathophysiologie der Schizophrenie spielen eben diese eine bedeutende Rolle und stellen somit Zielstrukturen für APs dar
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Harrold, Marc W. "Part 1, synthesis of trimetoquinol analogs as potential thromboxane A2 receptor antagonists ; Part 2, synthesis of permanently charged and permanently uncharged dopamine antagonists /." The Ohio State University, 1987. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487584612165271.

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"Effects of thromboxane A₂ receptor activation and periadventitial fat on cyclic GMP-dependent vaso-relaxation." 2007. http://library.cuhk.edu.hk/record=b5893260.

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Ho, Kwok Wa.<br>Thesis (M.Phil.)--Chinese University of Hong Kong, 2007.<br>Includes bibliographical references (leaves 60-65).<br>Abstracts in English and Chinese.<br>Chapter Chapter I<br>Chapter 1.1. --- Thromboxane A2 (TP) Receptors --- p.1<br>Chapter 1.1.1. --- Gene structure of human TP receptors --- p.1<br>Chapter 1.1.2. --- Isoforms of TP receptor --- p.1<br>Chapter 1.1.3. --- Distribution and expression of TP receptors in human --- p.2<br>Chapter 1.1.4. --- Signal transduction of TP receptors --- p.4<br>Chapter 1.1.5. --- Major agonists of TP receptor in animals and humans --- p.
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Book chapters on the topic "Thromboxane A2/blood"

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Becker, Richard C., and Frederick A. Spencer. "Aspirin." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0012.

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Aspirin, considered the prototypic platelet antagonist, has been available for over a century and currently represents a mainstay both in the prevention and treatment of vascular events that include stroke, myocardial infarction, peripheral vascular occlusion, and sudden death. Aspirin irreversibly acetylates cyclooxygenase (COX), impairing prostaglandin metabolism and thromboxane A2 (TXA2) synthesis. As a result, platelet aggregation in response to collagen, adenosine diphosphate (ADP), and thrombin (in low concentrations) is attenuated (Roth and Majerus, 1975). Because aspirin more selectively inhibits COX-1 activity (found predominantly in platelets) than COX-2 activity (expressed in tissues following an inflammatory stimulus), its ability to prevent platelet aggregation is seen at relatively low doses, compared with the drug’s potential antiinflammatory effects, which require much higher doses (Patrono, 1994). Several alternative mechanisms of platelet inhibition by aspirin have been proposed, including: (1) inhibition of platelet activation by neutrophils and (2) enhanced nitric oxide production. In addition, aspirin may prevent the progression of atherosclerosis by protecting low-density lipoprotein (LDL) cholesterol from oxidation and scavenging hydroxyl radicals. Following oral ingestion, aspirin is promptly absorbed in the proximal gastrointestinal (GI) tract (stomach, duodenum), achieving peak serum levels within 15 to 20 minutes and platelet inhibition within 40 to 60 minutes. Enteric-coated preparations are less well absorbed, causing an observed delay in peak serum levels and platelet inhibition to 60 and 90 minutes, respectively. The antiplatelet effect occurs even before acetylsalicylic acid is detectable in peripheral blood, probably from platelet exposure in the portal circulation. The plasma concentration of aspirin decays rapidly with a circulating half-life of approximately 20 minutes. Despite the drug’s rapid clearance, platelet inhibition persists for the platelet’s life span (7 ± 2 days) due to aspirin’s irreversible inactivation of COX-1. Because 10% of circulating platelets are replaced every 24 hours, platelet activity (bleeding time, primary hemostasis) returns toward normal (≥50% activity) within 5 to 6 days of the last aspirin dose (O’Brien, 1968). A single dose of 100 mg of aspirin effectively reduces the production of TXA2 in many (but not all) individuals.
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Conference papers on the topic "Thromboxane A2/blood"

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Van Nueten, J. M., W. J. Janssens, and F. De Clerck. "VASOCONSTRICTION IN RESPONSE TO HUMAN PLATELET-VESSEL WALL INTERACTIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644598.

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Human blood platelets, stimulated with thrombin, induced contractions of isolated basilar artery segments of the dog. These platelet-mediated vascular contractions were inhibited in a concentration-dependent way by flunarizine, a Ca2+-entry blocker, selective for vascular tissues. This inhibition increased gradually as a function of time after contact with flunarizine to reach its maximum after 60-90 min. Biochemical and pharmacological analyses, using the 5-HT2-serotonergic antagonist ritanserin, the thromboxane A2/prostaglandin endo-peroxide antagonist BM 13.177 and the fatty acid cyclo-oxyg
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McCollum, C. N., R. A. Harper, I. F. Lane, and A. C. Meek. "A SPECIFIC THROMBOXANE A2 ANTAGONIST, GR32191, REDUCES PLATELET DEPOSITION IN PTFE GRAFTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643753.

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Platelet inhibitory therapy improves patency in arterial grafts but when aspirin is given over 20% of patients discontinue therapy. We evaluated a specific Thromboxane A2 antagonist (GR32191 - Glaxo Group Research) on graft platelet uptake and pseudo-intimal hyperplasia in a canine model.Thirty greyhounds were randomised to orally administered placebo, GR32191 25mg, or aspirin150mg (ASA) plus dipyridamole 50mg (DPM) 12 hourly, commencing 48 hours prior to implantation of a 6cm length of 6mm-PTFE in the femoral artery. Autologous 111In-platelete were infused on the fifth postoperative day and p
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Kyrle, P. A., H. G. Eichler, and K. Lechner. "PROSTACYCLIN AND THROMBOXANE A2 GENERATION IN VIVO IN MAN -EFFECT OF LOW DOSE ASPIRIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643371.

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The effect of a low-dose aspirin regimen on platelet and vascular prostaglandin metabolism was studied in vivo in man. In a double-blind placebo-controlled cross-over study, 7 healthy male volunteers were treated with aspirin (35 mg.day−1 or placebo for 7 days. After a washout period of 2 weeks, the subject were crossed to the alternate treatment. 12 hours after the last dose of aspirin or placebo formation of thromboxane A2 (TxA2) and prostacyclin (FGI2) was measured in blood emerging from a standardized injury of the microvasculature made to determine bleeding time. TxA2 and PGI2 were measur
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McCabe, P. J., L. E. Stratton, E. J. Hornby, and M. Foster. "INHIBITION OF GUINEA-PIG PLATELET FUNCTION IN VIVO AND EX VIVO USING THE THROMBOXANE A2 ANTAGONISTS, AH23848 AND GR32191." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643468.

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The thromboxane A2 antagonist, GR32191 (Lumley et al., this meeting) was tested as an inhibitor of platelet aggregation in the guinea-pig and compared with another Tx-antagonist, AH23848 (Brittain et al, 1985). Guinea-pigs were dosed with AH23848 or GR32191 at 0.01-1.0mg/kg. At intervals, blood was taken and PRP was prepared for ex vivo aggregation studies. Collagen concentrations causing half maximal aggregation (IC50) were calculated for test and vehicle-dosed groups. Inhibition was expressed as a concentration ratio (IC50 test/IC50 vehicle). For in vivo studies, 111In-labelled platelets (12
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Wernet, P., M. Haurand, W. Nüsing, E. M. Schneider, K. Jaschonek, and V. Ullrich. "Production and characterization of a murine monoclonal antibody against human thromboxane synthetase." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643382.

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Eicosanoids appear to have an important role in the actual momentary regulation of tissue blood flow. The function of constricting blood vessels by affecting the vascular tone has been assigned to thromboxane. Thromboxane synthetase, the enzyme responsible for the conversion of Prostaglandin-H2 into thromboxane A2, has been shown to be present in platelets, lung fibroblasts and the brain. Recently, thromboxane synthetase has been totally purified. The enzyme isolated from platelets appears to have a molecular weight of 58,800 Dalton and to belong to the group of cytochrome P450 proteins. In or
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De Clerck, F., B. Xhonneux, L. Van Gorp, J. Beetens, and P. A. J. Janssen. "S2-SEROTONERGIC RECEPTOR INHIBITION (KETANSERIN), COMBINED WITH THROMBOXANE A2/PROSTAGLANDIN ENDOPEROXIDE RECEPTOR BLOCKADE (BM 13177) : ENHANCED ANTI-PLATELET EFFECT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643464.

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Subsequent to an initial activation, several products are released from the platelets, and -potentially- contribute to the recruitment of new cells to build up the eventual platelet haemostatic plug or thrombus. Among the various accussates, serotonin as well as the arachidonic acid derivatives thromboxane A2 (TXA2) and prostaglandin endoperoxides (PGEND) seem to be involved as causative mediators, in particular when acting in concert on the same target cells. Indeed, in vitro at concentrations achievable after oral administration to man, either ketanserin (K), an S2-serotonergic receptor anta
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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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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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Scharf, R. E., A. Wehmeier, and W. Schneider. "REDUCED PLATELET THROMBOXANE FORMATION IN ACUTE THROMBOTIC THROMBOCYTOPENIC PURPURA (TP): EVIDENCE FOR AN ABNORMAL PLATELET POPULATION WITH A TRANSIENT CYCLOOXYGENASE DEFECT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644588.

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We have recently shown that alpha-granule-depleted platelets circulate in acute TTP. These platelets are hemostatically defective due to partial loss of granular constituents and/or metabolic abnormalities. To further evaluate morphometric and metabolic changes of "exhausted" platelets, we studied their volume distribution and thromboxane A2 (TXA2) formation in a 35-year-old patient with primary TTP. Platelet volume distribution in whole blood was determined by the impedance method using citrate (0.38%)/glutaraldehyde (0.125%) as anticoagulant. TXB2 production was measured radioimmunologically
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Hansen, J. B., L. Wilsgard, J. O. Olsen, and B. Østerud. "A MODEL TO EVALUATE BLOOD CELLS BEHAVIOUR TO CELL ACTIVATION: A DIFFERENCE BETWEEN MEN AND WOMEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644627.

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This study was carried out to see what kind of response the blood cells have to a weak stimuli of lipopolysacc-harides (LPS), a substance that in small quantities may be a small part of the blood system. The parameters tested under this condition were: thromboxane A2 (TxA2) (produced in platelets), prostacyclin (PGI2) produced in white cells (mainly monocytes) and induced thromboplastin synthesis in monocytes.Heparinized blood from 40 men and 40 women was incubated with 2 ng LPS/ml blood for 2 hours. Blood cells were then either spun down to obtain plasma or mononuclear cells were isolated fro
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