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Journal articles on the topic 'Thromboxane A2/blood'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Cyrus, Tillmann, Yuemang Yao, Tao Ding, Jean Michel Dogné, and Domenico Praticò. "Thromboxane receptor blockade improves the antiatherogenic effect of thromboxane A2 suppression in LDLR KO mice." Blood 109, no. 8 (2006): 3291–96. http://dx.doi.org/10.1182/blood-2006-08-044990.

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Abstract Suppression of thromboxane (Tx) A2 biosynthesis retards atherogenesis. In this setting, the coincidental presence of nonconventional ligands for the TxA2 receptor (TP), such as isoprostanes, could still induce a proatherogenic vascular phenotype. However, no data are available on the effect of combining suppression of TxA2 formation with blockade of TP in atherogenesis. To this end, we tested the effect of a selective COX-1 inhibitor, SC560, a TP antagonist, BM-573, or a combination of both in low-density lipoprotein receptor-deficient mice on a high-fat diet. None of the treatments a

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12

Akkerman, Jan Willem N. "Neurotransmittors act as platelet activators." Blood 111, no. 2 (2008): 476. http://dx.doi.org/10.1182/blood-2007-10-116038.

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Thromboxane A2 and ADP act as important feedback activators of platelet function. The secretion of neuropeptides reveals a novel feedback loop that is not targeted specifically by aspirin and clopidogrel.

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13

Wacker, Michael J., Shaun R. Best, Lisa M. Kosloski, et al. "Thromboxane A2-induced arrhythmias in the anesthetized rabbit." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 4 (2006): H1353—H1361. http://dx.doi.org/10.1152/ajpheart.00930.2005.

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Experiments were conducted in the anesthetized rabbit to investigate mechanisms for arrhythmias that occur after left atrial injection of the thromboxane A2 (TxA2) mimetic U-46619. Arrhythmias were primarily of ventricular origin, dose dependent in frequency, and TxA2 receptor mediated. The response was receptor specific since arrhythmias were absent after pretreatment with a specific TxA2 receptor antagonist (SQ-29548) and did not occur in response to another prostaglandin, PGF2α. Alterations in coronary blood flow were unlikely the cause of these arrhythmias because coronary blood flow (as m

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14

Bresnahan, B. A., R. J. Roman, W. M. Bagchus, and E. A. Lianos. "Mesangial cell immune injury: effects of thromboxane receptor antagonism." Journal of the American Society of Nephrology 1, no. 8 (1991): 1041–47. http://dx.doi.org/10.1681/asn.v181041.

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We assessed the renal hemodynamic changes occurring acutely after glomerular mesangial cell immune injury and the effects of thromboxane receptor antagonism on these changes. A single intravenous proteinuric dose of a monoclonal antibody raised against the rat thymocyte antigen Thy 1.1 (ER4), which is also expressed in rat mesangial cells, induced acute decrements in glomerular filtration rate and in renal blood flow in male Munich-Wistar rats. One hour after administration of 4 to 6 mg/kg of ER4 antibody, glomerular filtration rate and renal blood flow decreased by 80 and 36%, respectively. T

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15

Brace, L. D., D. L. Venton, and G. C. Le Breton. "Thromboxane A2/prostaglandin H2 mobilizes calcium in human blood platelets." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 1 (1985): H1—H7. http://dx.doi.org/10.1152/ajpheart.1985.249.1.h1.

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The present study investigated the mechanism by which thromboxane A2/prostaglandin H2 (TXA2/PGH2) stimulates platelet activation. Previous studies in isolated platelet vesicles have suggested that TXA2/PGH2 functions to release calcium from intraplatelet stores. On this basis, we investigated whether TXA2/PGH2 causes mobilization of calcium in intact platelets. Calcium redistribution was measured using the fluorescent probe, chlortetracycline (CTC), and a photon-counting microspectrofluorometer. Human platelet-rich plasma was incubated with CTC (50 microM) for 40 min at 25 degrees C. Shape cha

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16

Peters, A. M., I. F. Lane, M. Sinclair, J. T. C. Irwin, and C. N. McCollum. "The Effects of Thromboxane Antagonism on the Transit Time of Platelets Through the Spleen." Thrombosis and Haemostasis 54, no. 02 (1985): 495–97. http://dx.doi.org/10.1055/s-0038-1657881.

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SummaryThe spleen is well-known as a site for platelet pooling, although the mechanisms controlling intrasplenic platelet transit are essentially unknown. We tested the possibility that thromboxane A2 might be involved in this control by measuring intrasplenic platelet transit time in 10 subjects receiving a specific thromboxane A2 receptor antagonist (AH23848B; 70 mg; Glaxo Group Research Ltd), in 10 receiving aspirin (300 mg) plus dipyridamole (75 mg), and in 9 receiving placebo. All doses were administered 3 times daily commencing 4 days prior to transit time measurement.Mean intrasplenic p

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17

Cirino, M., H. Morton, C. MacDonald, J. Hadden, and A. W. Ford-Hutchinson. "Thromboxane A2 and prostaglandin endoperoxide analogue effects on porcine renal blood flow." American Journal of Physiology-Renal Physiology 258, no. 1 (1990): F109—F114. http://dx.doi.org/10.1152/ajprenal.1990.258.1.f109.

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Thromboxane A2 (TxA2) has been implicated as a mediator of renal and cardiovascular diseases. However, the direct effects of TxA2 on the renal system have been difficult to study because of the instability of the agonist. In the present study injection of synthetic TxA2 directly into the renal artery of anesthetized pigs produced dose-related decreases in renal blood flow (RBF) from 101 +/- 11 to 12 +/- 3 ml/min at the highest dose (20 ng/kg). The reductions in RBF were similar to those produced by the stable prostaglandin endoperoxide analogue, U-44069, although TxA2 was three times more pote

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18

Pozgajova, Miroslava, Judith Cosemans, Imke Munnix та ін. "Role of murine integrin α2β1 in thrombus stabilization and embolization: Contribution of thromboxane A2". Thrombosis and Haemostasis 98, № 11 (2007): 1072–80. http://dx.doi.org/10.1160/th07-02-0089.

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SummaryPlatelets stably interact with collagen via glycoprotein (GP)VI and α2β1 integrin. With α2-null mice, we investigated the role of α2β1 in thrombus formation and stability in vivo and in vitro. Using a FeCl3-induced thrombosis model, in arteries from α2-null mice smaller thrombi were formed with more embolization compared to vessels from wild-type mice. Aspirin treatment of wild-type mice causes similar effects, while the thromboxane A2 analogue U46619 was borderline effective in suppressing the embolisation in α2-null mice. In vitro, perfusion of α2-null blood over collagen resulted in

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19

Martin, S. E., J. T. Kuvin, S. Offenbacher, B. M. Odle, and R. E. Patterson. "Neuropeptide Y and coronary vasoconstriction: role of thromboxane A2." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 4 (1992): H1045—H1053. http://dx.doi.org/10.1152/ajpheart.1992.263.4.h1045.

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We previously reported that coronary constriction following neuropeptide Y (NPY) was alleviated by cyclooxygenase blockade. To determine the role of thromboxane A2 (TxA2), anesthetized dogs received two paired doses of NPY given 2 h apart. Nine control dogs received NPY alone. Nine test dogs received one of three TxA2 receptor antagonists given between the doses of NPY. Also, five dogs received NPY during which prostaglandins were measured. In controls, NPY decreased coronary blood flow and increased aortic pressure; coronary resistance was increased significantly. Heart rate fell, and myocard

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20

Ushikubi, Fumitaka, Masatoshi Nakajima, Minoru Okuma, Shuh Narumiya, and Motohatsu Fujiwara. "Thromboxane A2 receptor in human blood platelets. 1. Purification and properties." Japanese Journal of Pharmacology 49 (1989): 141. http://dx.doi.org/10.1016/s0021-5198(19)56266-7.

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21

Pal, Saumen, Jing Wu, Justin K. Murray, et al. "An antiangiogenic neurokinin-B/thromboxane A2 regulatory axis." Journal of Cell Biology 174, no. 7 (2006): 1047–58. http://dx.doi.org/10.1083/jcb.200603152.

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Establishment of angiogenic circuits that orchestrate blood vessel development and remodeling requires an exquisite balance between the activities of pro- and antiangiogenic factors. However, the logic that permits complex signal integration by vascular endothelium is poorly understood. We demonstrate that a “neuropeptide,” neurokinin-B (NK-B), reversibly inhibits endothelial cell vascular network assembly and opposes angiogenesis in the chicken chorioallantoic membrane. Disruption of endogenous NK-B signaling promoted angiogenesis. Mechanistic analyses defined a multicomponent pathway in whic

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22

Toth, Balazs, Yukihiro Yokoyama, Martin G. Schwacha, et al. "Insights into the role of interleukin-6 in the induction of hepatic injury after trauma-hemorrhagic shock." Journal of Applied Physiology 97, no. 6 (2004): 2184–89. http://dx.doi.org/10.1152/japplphysiol.00499.2004.

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Although systemic interleukin-6 (IL-6) level is elevated, hepatocellular function is impaired and liver injury occurs after trauma-hemorrhage (T-H), it remains unknown whether a causal relationship exists between elevated IL-6 levels and liver injury after T-H. We hypothesized that IL-6 is causative in the development of hepatic dysfunction and injury after T-H. To examine this, adult male Sprague-Dawley rats underwent a 5-cm midline laparotomy and were subjected to hemorrhagic shock (blood pressure = 35 mmHg for ∼90 min), followed by resuscitation (Ringer lactate, 4 times the shed blood volum

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Cattaneo, Marco, Christian Gachet, Jeanne-Pierre Cazenave, and Marian A. Packham. "Adenosine diphosphate (ADP) does not induce thromboxane A2 generation in human platelets." Blood 99, no. 10 (2002): 3868–70. http://dx.doi.org/10.1182/blood-2002-01-0313.

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Naik, Meghna U., Pravin Patel, Randall Derstine, et al. "Ask1 regulates murine platelet granule secretion, thromboxane A2 generation, and thrombus formation." Blood 129, no. 9 (2017): 1197–209. http://dx.doi.org/10.1182/blood-2016-07-729780.

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Key Points ASK1 regulates TxA2 generation through p38 MAPK-dependent phosphorylation of cPLA2. Because of impaired platelet function, Ask1−/− mice are protected from arterial thrombosis and pulmonary thromboembolism.

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25

Habazettl, H., P. F. Conzen, B. Vollmar, E. Yekebas, and K. Peter. "Effect of leukopenia on pulmonary hypertension after heparin-protamine in pigs." Journal of Applied Physiology 73, no. 1 (1992): 44–49. http://dx.doi.org/10.1152/jappl.1992.73.1.44.

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Heparin neutralization by protamine after cardiac surgery and cardiopulmonary bypass may be associated with complement activation, transient leukopenia, thromboxane A2 release, and severe pulmonary hypertension. The role of leukocytes in the heparin-protamine reaction was studied in leukopenic pigs (n = 9) and a control group (n = 8). Leukopenia was induced by pretreatment with cyclophosphamide (30 mg.kg-1.day-1) for 6–7 days. During general anesthesia and after catheterization, baseline recordings of hemodynamics were performed and blood samples were withdrawn. Heparin (250 IU/kg) was injecte

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26

Ushikubi, F., M. Nakajima, M. Hirata, M. Okuma, M. Fujiwara, and S. Narumiya. "Purification of the thromboxane A2/prostaglandin H2 receptor from human blood platelets." Journal of Biological Chemistry 264, no. 28 (1989): 16496–501. http://dx.doi.org/10.1016/s0021-9258(19)84733-6.

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27

Sun-Ok, Kim, Lim Chang T., Stephen C.-T. Lam, et al. "Purification of the human blood platelet thromboxane A2/prostaglandin H2 receptor protein." Biochemical Pharmacology 43, no. 2 (1992): 313–22. http://dx.doi.org/10.1016/0006-2952(92)90294-s.

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28

ohtsu, Kunishige, Fumitaka Ushikubi, Yoshiharu Kimura, Minoru Okuma, Shuh Narumiya, and Motohatsu Fujiwara. "Thromboxane A2 receptor in human blood platelet 2. Synthesis of photoaffinity labels." Japanese Journal of Pharmacology 46 (1988): 279. http://dx.doi.org/10.1016/s0021-5198(19)57677-6.

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Wacker, M. J., H. L. Wilhelm, S. E. Gomez, E. Floor, and J. A. Orr. "Role of serotonin in thromboxane A2-induced coronary chemoreflex." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 3 (2003): H867—H875. http://dx.doi.org/10.1152/ajpheart.00617.2002.

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We reported previously that the thromboxane A2 (TxA2) mimetic U-46619 stimulates cardiac vagal afferent nerves, eliciting a reflex decrease in heart rate (HR) and arterial blood pressure (ABP). The present experiments were designed to test the hypothesis that TxA2evokes these changes via the release of serotonin [5-hydroxytryptamine (5-HT)] and activation of the 5-HT3receptor. Injections of the 5-HT3 antagonist tropisetron (1 mg of 3-tropanyl-indole-3-carboxylate or ICS-205-930) attenuated the decreases in HR and ABP induced by left atrial injections of U-46619 (20 μg). Tropisetron administrat

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Boussairi, E. H., J. Sacquet, J. Sassard, and D. Benzoni. "Thromboxane A2-prostaglandin H2 and renovascular hypertension in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 5 (1994): R1190—R1197. http://dx.doi.org/10.1152/ajpregu.1994.267.5.r1190.

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To evaluate the contribution of thromboxane (Tx) A2-prostaglandin (PG) H2 in two-kidney, one-clip Goldblatt hypertension (GH), 26 GH rats were chronically treated (GHT) with a specific TxA2-PGH2 receptor antagonist, CGS-22652 (30 mg.kg-1.24 h-1 sc); 28 others as well as 17 sham-clipped (SC) rats received vehicle. Twelve GH and 3 GHT rats developed malignant hypertension and died. After 6 wk of treatment, GH rats exhibited higher mean blood pressure (BP; 189 +/- 3 vs. 118 +/- 2 mmHg) and an increased vascular reactivity to the main pressor agents compared with SC rats. Chronic TxA2-PGH2 recepto

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Clerck, F. De, J. Beetens, D. de Chaffoy de Courcelles, E. Freyne, and P. A. J. Janssen. "R 68 070: Thromboxane A2 Synthetase Inhibition and Thromboxane A2/Prostaglandin Endoperoxide Receptor Blockade Combined in One Molecule - I. Biochemical Profile In Vitro." Thrombosis and Haemostasis 61, no. 01 (1989): 035–42. http://dx.doi.org/10.1055/s-0038-1646523.

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SummaryR 68 070 or (E)-5-[[[(3-pyridinyl)[3-(trifluoromethyl)phenyl]- methylen]amino]oxy] pentanoic acid (Janssen Research Foundation, Belgium) combines specific thromboxane A2 (TXA2) synthetase inhibition with TXA2/prostaglandin endoperoxide receptor blockade in one molecule.In vitro, the compound specifically inhibits the production of TXB2 from [14C] arachidonic acid by washed human platelets (IC50 = 8.2 × 10-9 M) and by platelet microsomes (IC50 = 3.6 × 10-9 M), of MDA (IC50 = 1.91 × 10-8 M) and of TXB2 (IC50 = 1.47 × 10-8 M) by thrombin-coagulated human platelet-rich plasma (P.R.P.) and w

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Ang, Darwin, Stan Kurek, Mark Mckenney, et al. "Outcomes of Geriatric Trauma Patients on Preinjury Anticoagulation: A Multicenter Study." American Surgeon 83, no. 6 (2017): 527–35. http://dx.doi.org/10.1177/000313481708300614.

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Outpatient anticoagulation in the geriatric trauma patient is a challenging clinical problem. The aim of this study is to determine clinical outcomes associated with class of preinjury anticoagulants (PA) used by this population. This is a multicenter retrospective cohort study among four Level II trauma centers. A total of 1642 patients were evaluated; 684 patients were on anticoagulation and 958 patients were not. Patients on PA were compared with those who were not. Drug classes were divided into thromboxane A2 inhibitors, vitamin K factor-dependent inhibitors, antithrombin III activation,

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Morinelli, T. A., A. K. Okwu, D. E. Mais, et al. "Difluorothromboxane A2 and stereoisomers: stable derivatives of thromboxane A2 with differential effects on platelets and blood vessels." Proceedings of the National Academy of Sciences 86, no. 14 (1989): 5600–5604. http://dx.doi.org/10.1073/pnas.86.14.5600.

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Undas, Anetta, Kathleen E. Brummel-Ziedins, and Kenneth G. Mann. "Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions." Blood 109, no. 6 (2006): 2285–92. http://dx.doi.org/10.1182/blood-2006-01-010645.

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Abstract Aspirin is effective in the prevention of cardiovascular events in high-risk patients. The primary established effect of aspirin on hemostasis is to impair platelet aggregation via inhibition of platelet thromboxane A2 synthesis, thus reducing thrombus formation on the surface of the damaged arterial wall. Growing evidence also indicates that aspirin exerts additional antithrombotic effects, which appear to some extent unrelated to platelet thromboxane A2 production. Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as

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Murugappan, Swaminathan, Haripriya Shankar, Surya Bhamidipati, Robert T. Dorsam, Jianguo Jin та Satya P. Kunapuli. "Molecular mechanism and functional implications of thrombin-mediated tyrosine phosphorylation of PKCδ in platelets". Blood 106, № 2 (2005): 550–57. http://dx.doi.org/10.1182/blood-2004-12-4866.

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Abstract Thrombin has been known to cause tyrosine phosphorylation of protein kinase C δ (PKCδ) in platelets, but the molecular mechanisms and function of this tyrosine phosphorylation is not known. In this study, we investigated the signaling pathways used by protease-activated receptors (PARs) to cause tyrosine phosphorylation of PKCδ and the role of this event in platelet function. PKCδ was tyrosine phosphorylated by either PAR1 or PAR4 in a concentration- and time-dependent manner in human platelets. In particular, the tyrosine 311 residue was phosphorylated downstream of PAR receptors. Al

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Garcia, Analia, Todd M. Quinton, Robert T. Dorsam, and Satya P. Kunapuli. "Src family kinase–mediated and Erk-mediated thromboxane A2 generation are essential for VWF/GPIb-induced fibrinogen receptor activation in human platelets." Blood 106, no. 10 (2005): 3410–14. http://dx.doi.org/10.1182/blood-2005-05-1933.

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AbstractThe binding of von Willebrand factor (VWF) to the platelet membrane glycoprotein Ib-IX (GPIb-IX) results in platelet activation. In this study, we sought to clarify previous conflicting reports and to elucidate the mechanism of activation and the precise role of extracellular signal-regulated kinase (Erk) in VWF-induced platelet activation. Erk2 is activated in platelets on stimulation with VWF/ristocetin in a time-dependent manner. VWF-induced Erk2 phosphorylation and thromboxane A2 (TXA2) release were completely blocked by PP2, an Src family kinase inhibitor, suggesting that Erk is d

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Chueh, Tsung-Hung, Yu-Hsiuan Cheng, Kuo-Hsin Chen, and Chiang-Ting Chien. "Thromboxane A2 Synthase and Thromboxane Receptor Deletion Reduces Ischaemia/Reperfusion-Evoked Inflammation, Apoptosis, Autophagy and Pyroptosis." Thrombosis and Haemostasis 120, no. 02 (2019): 329–43. http://dx.doi.org/10.1055/s-0039-3400304.

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Abstract Aim Enhancement of thromboxane A2 (TXA2) synthase (TXAS) activity, TXA2 release, and thromboxane prostanoid (TP) receptor activation leads to vasoconstriction and oxidative injury. We explored whether genetic deletion of TXAS/TXA2/TP signalling may reduce renal ischaemia/reperfusion (I/R) injury in mice. Materials and Methods Renal haemodynamics and function were evaluated in TXAS+/+TP+/+ (wild-type, WT), TXAS−/− (TXS−/−), TP−/− and TXAS−/−TP−/− (double knockout, dKO) mice in response to intravenous TXA2 mimetic-U46619 and 45-minute renal ischaemia and 4-hour reperfusion injury. We ex

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Kramer, Herbert J., Kriemhild Schwarting, and Angela Bäcker. "Impaired Renal Function in Obstructive Jaundice: Enhanced Glomerular Thromboxane Synthesis and Effects of Thromboxane Receptor Blockade in Bile Duct-Ligated Rats." Clinical Science 88, no. 1 (1995): 39–45. http://dx.doi.org/10.1042/cs0880039.

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1. Patients with obstructive jaundice are especially susceptible to acute renal failure. We have previously observed that in rats with bile duct ligation impaired renal function is associated with increased urinary thromboxane excretion. 2. In the present study we therefore investigated, in rats with bile duct ligation, renal function, urinary thromboxane excretion and thromboxane B2 synthesis by isolated glomeruli as well as the effects of the thromboxane A2/prostaglandin H2 receptor antagonist Daltroban on renal function in rats with bile duct ligation as compared with sham-operated rats. 3.

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Newman, J. H., B. J. Butka, and K. L. Brigham. "Thromboxane A2 and prostacyclin do not modulate pulmonary hemodynamics during exercise in sheep." Journal of Applied Physiology 61, no. 5 (1986): 1706–11. http://dx.doi.org/10.1152/jappl.1986.61.5.1706.

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The purpose of this study was to determine the role of thromboxane and prostacyclin in modulating pulmonary hemodynamics during maximal cardiopulmonary stress in the healthy lung. We studied 11 yearling sheep in paired studies during progressive maximal treadmill exercise with and without meclofenamate (n = 5), ibuprofen (n = 6), or UK38485 (n = 2). We also studied five sheep during hypoxia and hypoxic exercise, and six sheep during prolonged steady-state treadmill exercise for 45-60 min with and without drug treatment. We measured the metabolites of thromboxane A2 (thromboxane B2, TxB2) and p

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Dotevall, Annika, Christina Rångemark, Elsa Eriksson, Jack Kutti, Hans Wadenvik, and Åke Wennmalm. "Cigarette Smoking Increases Thromboxane A2 Formation without Affecting Platelet Survival in Young Healthy Females." Thrombosis and Haemostasis 68, no. 05 (1992): 583–88. http://dx.doi.org/10.1055/s-0038-1646321.

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SummarySmoking is a risk factor for the development of atherosclerotic cardiovascular disease, in men as well as in women. An increased urinary excretion of the thromboxane metabolite 2,3-dinor-thromboxane B2 (Tx-M) has been observed in smokers of both genders, suggesting that cigarette smoking may facilitate cardiovascular disease via an action on the platelets. The present study addressed the hypothesis that the increased Tx-M excretion in female smokers reflects a true facilitation of platelet reactivity in vivo, rather than an increased destruction of the platelets. In healthy female volun

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Kalichman, M. W., M. T. Sanicolas, M. C. Jorge, and L. Roux. "Effects of cocaine on blood flow and prostaglandin metabolites in rat sciatic nerve." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 6 (1994): H2515—H2519. http://dx.doi.org/10.1152/ajpheart.1994.266.6.h2515.

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To better understand the mechanisms of local anesthetic-reduced nerve blood flow and nerve blood flow regulation, the effects of cocaine on blood flow and vasoactive prostaglandins were tested in the sciatic nerve of anesthetized rats. After 30 min, nerve blood flow was significantly reduced from baseline by perineural injection of 160 mM cocaine [-29.4 +/- 4.0 (SD) laser-Doppler flow units (P < 0.001)] but not saline (1.6 +/- 11.3). These same nerves were removed and assayed for the stable metabolites 6-ketoprostaglandin F1 alpha and thromboxane B2 of the vasoactive eicosanoids prostacycli

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Weber, C., J. R. Beetens, F. Tegtmeier, et al. "Ridogrel Inhibits Systemic and Renal Formation of Thromboxane A2 and Antagonizes Platelet Thromboxane A2/Prostaglandin Endoperoxide Receptors upon Chronic Administration to Man." Thrombosis and Haemostasis 68, no. 02 (1992): 214–20. http://dx.doi.org/10.1055/s-0038-1656351.

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SummaryThe effects of ridogrel, a dual thromboxane A2 (TXA2) synthase inhibitor and TXA2/prostaglandin (PG) endoperoxide receptor antagonist, on systemic and renal production of prostaglandins and on platelet TXA2/PG endoperoxide receptors was evaluated upon chronic administration (300 mg b. i. d. orally, for 8 and 29 days) to man. Such a medication with ridogrel inhibits the systemic as well as the renal production of TXA2 as measured by the urinary excretion of 2,3-dinor-TXB2 and TXB2 respectively without inducing significant changes in systemic or renal PGI2 production. Simultaneously with

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Gegenbauer, Kristina, Giuliano Elia, Alfonso Blanco-Fernandez, and Albert Smolenski. "Regulator of G-protein signaling 18 integrates activating and inhibitory signaling in platelets." Blood 119, no. 16 (2012): 3799–807. http://dx.doi.org/10.1182/blood-2011-11-390369.

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Abstract Regulator of G-protein signaling 18 (RGS18) is a GTPase-activating protein for the G-α-q and G-α-i subunits of heterotrimeric G-proteins that turns off signaling by G-protein coupled receptors. RGS18 is highly expressed in platelets. In the present study, we show that the 14-3-3γ protein binds to phosphorylated serines 49 and 218 of RGS18. Platelet activation by thrombin, thromboxane A2, or ADP stimulates the association of 14-3-3 and RGS18, probably by increasing the phosphorylation of serine 49. In contrast, treatment of platelets with prostacyclin and nitric oxide, which trigger in

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Kintner, D. B., P. W. Kranner, and D. D. Gilboe. "Cerebral Vascular Resistance following Platelet and Leukocyte Removal from Perfusate." Journal of Cerebral Blood Flow & Metabolism 6, no. 1 (1986): 52–58. http://dx.doi.org/10.1038/jcbfm.1986.7.

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The rapid increases in cerebral vascular resistance (CVR) frequently observed during extracorporeal perfusion of isolated organs with whole or diluted blood have been investigated using the isolated canine brain preparation. Our data strongly suggest that these increases are caused by a vasoconstrictor that is present in the buffy coat. Plasma serotonin levels were measured and found to be insignificant after conditioning and storage. Conditioning the blood reduced the platelets and the potential for thromboxane A2 production to ∼40% of normal. However, there was no correlation between thrombo

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Harding, P., C. Stonier, and G. M. Aber. "Effect of angiotensin-converting enzyme inhibitors on glomerular eicosanoid production in normotensive and spontaneously hypertensive rats." Clinical Science 81, s25 (1991): 491–97. http://dx.doi.org/10.1042/cs0810491.

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1. This study was designed to examine the production of certain eicosanoids (prostaglandin E2), prostacyclin (as 6-keto-prostaglandin F1α) and thromboxane A2 (as thromboxane B2) by glomeruli isolated from normotensive Wistar-Kyoto and spontaneously hypertensive rats both before and after the administration of one of three angiotensin-converting enzyme inhibitors, captopril, enalapril or fosinopril, for 10 days. 2. Measurements of glomerular eicosanoid production were made under basal conditions and in the presence of excess exogenous arachidonic acid. 3. The production of prostaglandin E2, 6-k

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Hansen, John-Bjarne, Line Wilsgård, Jan Ole Olsen, Birgit Svensson, and Bjarne Østerud. "The Effect of Lipopolysaccharides (LPS) on Generation of Thromboxane A2 and Thromboplastin Activity in Whole Blood of Males, Females and Females on Oral Contraceptives." Thrombosis and Haemostasis 61, no. 03 (1989): 493–96. http://dx.doi.org/10.1055/s-0038-1646621.

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SummaryHeparinized blood sample taken from 81 healthy persons, 40 men and 41 women of whom 17 were on combined oral contraceptives, were incubated with 2 ng lipopolysaccharides (LPS)/ml blood. Quantitation of thromboxane B2 (TxB2) in the resultant plasma revealed a significantly (p <0.001) higher generation of TxB2 in men than in women. No sexual differences were observed in thromboplastin activity in unstimulated and LPS stimulated monocytes. Addition of liposomes together with LPS enhanced the synthesis of thromboplastin 2-10 fold and unveiled a higher synthesis of thromboplastin among me

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Borg, Catherine, Stephen C.-T. Lam, Jeanette P. Dieter, et al. "Anti-peptide antibodies against the human blood platelet thromboxane A2/prostaglandin H2 receptor." Biochemical Pharmacology 45, no. 10 (1993): 2071–78. http://dx.doi.org/10.1016/0006-2952(93)90018-r.

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Lad, N., D. O. Lunt, and D. P. Tuffin. "The effect of thromboxane a2 systhesis inhibitors on platelet aggregation in whole blood." Thrombosis Research 46, no. 4 (1987): 555–66. http://dx.doi.org/10.1016/0049-3848(87)90156-3.

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Ren, Rendong, Takashi Hashimoto, Masashi Mizuno, et al. "A lipid peroxidation product 9-oxononanoic acid induces phospholipase A2 activity and thromboxane A2 production in human blood." Journal of Clinical Biochemistry and Nutrition 52, no. 3 (2013): 228–33. http://dx.doi.org/10.3164/jcbn.12-110.

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Kraft, S. A., S. Fujishima, G. P. McGuire, J. S. Thompson, T. A. Raffin, and R. G. Pearl. "Effect of blood and albumin on pulmonary hypertension and edema in perfused rabbit lungs." Journal of Applied Physiology 78, no. 2 (1995): 499–504. http://dx.doi.org/10.1152/jappl.1995.78.2.499.

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Perfusate composition may alter pulmonary hemodynamics and edema formation in perfused lungs. Perfusion for 3 h with Krebs-Henseleit solution with 3% bovine serum albumin did not produce pulmonary hypertension, pulmonary edema (assessed by lung wet-to-dry wt ratio), or increased macromolecular permeability (assessed by 125I-albumin uptake). Addition of blood to hematocrit levels of 10 or 20% resulted in pulmonary hypertension during the final hour of perfusion but not pulmonary edema or increased macromolecular permeability. Pulmonary hypertension during blood perfusion was primarily due to in

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