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Relevant bibliographies by topics / Platelet activating factor. Arachidonic acid

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Academic literature on the topic 'Platelet activating factor. Arachidonic acid'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Platelet activating factor. Arachidonic acid"

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Holub, Bruce J., Diana J. Philbrick, Anwar Parbtani, and William F. Clark. "Dietary lipid modification of renal disorders and ether phospholipid metabolism." Biochemistry and Cell Biology 69, no. 7 (1991): 485–89. http://dx.doi.org/10.1139/o91-072.

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The formation of arachidonic acid derived eicosanoids, including thromboxane A2 and leukotriene B4, as well as platelet-activating factor (1-O-alkyl-2-acetyl-glycerophosphocholine), has been implicated in various renal pathophysiologies. Alteration of the fatty acid composition of membrane phospholipids in platelets, the glomerulus, and inflammatory cells, and of 1-O-alkyl-2-acyl-glycerophosphocholine (platelet-activating factor precursor) can be attained by dietary lipid modifications (e.g., consumption of fish oil containing n – 3 polyunsaturated fatty acids). These changes have been associa

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IZAKI, S., T. YAMAMOTO, Y. GOTO, et al. "Platelet-activating factor and arachidonic acid metabolites in psoriatic inflammation." British Journal of Dermatology 134, no. 6 (1996): 1060–64. http://dx.doi.org/10.1111/j.1365-2133.1996.tb07943.x.

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IZAKI, S., T. YAMAMOTO, Y. GOTO, et al. "Platelet-activating factor and arachidonic acid metabolites in psoriatic inflammation." British Journal of Dermatology 134, no. 6 (1996): 1060–64. http://dx.doi.org/10.1046/j.1365-2133.1996.d01-902.x.

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Nakajima, Toshiaki, Tsuneaki Sugimoto, and Yoshihisa Kurachi. "Platelet-activating factor activates cardiac GK via arachidonic acid metabolites." FEBS Letters 289, no. 2 (1991): 239–43. http://dx.doi.org/10.1016/0014-5793(91)81079-n.

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Bin, Zhang, and Long Kun. "Inhibition by Glaucocalyxin A of Aggregation of Rabbit Platelets Induced by ADP, Arachidonic Acid and Platelet-Activating Factor, and Inhibition of [3H]-PAF Binding." Thrombosis and Haemostasis 67, no. 04 (1992): 458–60. http://dx.doi.org/10.1055/s-0038-1648470.

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SummaryGlaucocalyxin A is a new diterpenoid isolated from the ethereal extract of the leaves of Rabdosia japonica (Burm f) Hara var glaucocalyx (Maxim) Hara (Labiatae) collected in the northeastern China. When it was incubated with washed rabbit platelets, glaucocalyxin A inhibited ADP- or arachidonic acid-induced platelet aggregation with IC50 values of 4.4 μmol/1, 14.1 μmol/1 respectively. Glaucocalyxin A also inhibited PAF-induced aggregation of rabbit platelets which were refractory to ADP and arachidonic acid with an IC50 value of 13.7 μmol/1. Analysis of [3H]-PAF binding showed that glau

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Ahmed, Y., M. H. F. Sullivan, and M. G. Elder. "Detection of Platelet Desensitization in Pregnancy-Induced Hypertension Is Dependent on the Agonist Used." Thrombosis and Haemostasis 65, no. 05 (1991): 474–77. http://dx.doi.org/10.1055/s-0038-1648174.

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SummaryThe aggregation of platelets from women with pregnancy-induced hypertension (P.I.H.), or with normal pregnancies, in response to arachidonic acid, ADP, collagen or platelet activating factor (PAF) was examined. No differences in platelet aggregation between the normotensive and hypertensive women were detected when arachidonic acid or collagen were used to stimulate in vitro platelet aggregation. Higher concentrations of ADP and PAF were required to aggregate platelets from women with P.I.H. compared with platelets from normotensive controls. Platelets from women with normotensive pregn

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Saeed, S. A., R. U. Simjee, G. Shamim, and A. H. Gilani. "Eugenol: a dual inhibitor of platelet-activating factor and arachidonic acid metabolism." Phytomedicine 2, no. 1 (1995): 23–28. http://dx.doi.org/10.1016/s0944-7113(11)80044-9.

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Ramesha, C. S., and W. C. Pickett. "Metabolism of platelet-activating factor by arachidonic acid-depleted rat polymorphonuclear leukocytes." Journal of Biological Chemistry 261, no. 33 (1986): 15519–23. http://dx.doi.org/10.1016/s0021-9258(18)66744-4.

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Livio, M., G. Vigano, M. Morigi, A. Ubiali, M. Galbusera, and G. Remuzzi. "Role of platelet-activating factor in primary hemostasis." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 6 (1988): H1218—H1223. http://dx.doi.org/10.1152/ajpheart.1988.254.6.h1218.

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To determine whether platelet-activating factor (PAF) has a physiological role in the process of primary hemostasis in the rabbit, we measured skin bleeding times in animals given orally a specific PAF-receptor antagonist L-652,731. One hour after the administration of L-652,731 (20 or 40 mg/kg), a significant prolongation of bleeding time was observed. Parameters known to interfere with the process of primary hemostasis were not altered by PAF-receptor antagonist. In addition, no changes were observed in platelet count and vessel wall arachidonic acid metabolism, as revealed by serum thrombox

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Garcia, M. D. C., S. Fernandez-Gallardo, M. A. Gijon, C. Garcia, M. L. Nieto, and M. Sanchez Crespo. "Biosynthesis of platelet-activating factor (PAF) in human polymorphonuclear leucocytes. The role of lyso-PAF disposal and free arachidonic acid." Biochemical Journal 268, no. 1 (1990): 91–98. http://dx.doi.org/10.1042/bj2680091.

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Theophylline and 1-methyl-3-isobutylxanthine (MIX), compounds that block eicosanoid formation and modulate phospholipase A2 activity, inhibited in a dose-dependent manner the formation of both leukotriene B4 (LTB4) and platelet-activating factor (PAF) by human polymorphonuclear leucocytes (PMN) in response to ionophore A23187. Theophylline and MIX lacked any inhibitory effect on acetyl-CoA: lyso-PAF acetyltransferase activity, which is the rate-limiting step for PAF biosynthesis in PMN. The effect of theophylline and MIX on PAF formation could be reversed by incubating the cells in the presenc

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Dissertations / Theses on the topic "Platelet activating factor. Arachidonic acid"

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Usman, Rukhsana. "Platelet activity and arachidonic acid metabolism: modulation by factors in plasma and cerebrospinal fluidand by diet." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31233934.

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Usman, Rukhsana. "Platelet activity and arachidonic acid metabolism : modulation by factors in plasma and cerebrospinal fluid and by diet /." [Hong Kong] : University of Hong Kong, 1994. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13787263.

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Benhamou, Marc. "Etude des recepteurs fc des mastocytes derives de la moelle osseuse de souris : modulation du fc::(e)r1 par la dexametasone, et caracterisation du fc::(g)r." Paris 7, 1988. http://www.theses.fr/1988PA077009.

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Lai, Christopher Kei Wai. "The role of 15-(s)-Hydroxyeicosatetraenoic acid and platelet activating factor in the pathogenesis of bronchial asthma." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316419.

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Liu, Langni. "Ultraviolet-B radiation induces release of bioactive microvesicle particles in keratinocytes via platelet-activating factor and acid sphingomyelinase." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1598672100210086.

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Awoyemi, Azeezat Afolake. "Regulation of Microvesicle Particle release in keratinocytes." Wright State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=wright1533682055929687.

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Fahy, Katherine Erin. "Thermal Burn Injury Induced Microvesicle Particle Release." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright149383031006972.

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Thapa, Pariksha. "Kinetics of Microvesicle Particle Release in Keratinocytes." Wright State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=wright1566504910360327.

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Books on the topic "Platelet activating factor. Arachidonic acid"

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Arachidonate Related Lipid Mediators, Volume 187: Volume 187: Arachidonate Related Lipid Mediators (Methods in Enzymology). Academic Press, 1990.

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C, Murphy Robert, and Fitzpatrick Frank A, eds. Arachidonate related lipid mediators. Academic Press, 1990.

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Book chapters on the topic "Platelet activating factor. Arachidonic acid"

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Parratt, J. R., and N. Pacitti. "The Possible Roles of Lipoxygenase Products of Arachidonic Acid Metabolism and of Platelet Activating Factor in Shock." In Septic Shock. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83108-9_7.

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Jean Ammit, Alaina, and Chris O’Neill. "Platelet-Activating Factor (PAF) Receptor Antagonists Inhibit Arachidonic Acid Induced Platelet Aggregation in Rabbit Whole Blood." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch45.

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Chilton, Floyd, Marc Cluzel, and Massimo Triggiani. "Recent Advances in Our Understanding of the Biochemical Interactions Between Platelet-Activating Factor and Arachidonic Acid." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch11.

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Hanahan, Donald J. "Minor Phospholipids: Platelet activating factor (PAF) and PAF analogs, Lysophosphatidic acid and phosphatidic acid, Phosphatidylglycerol, Cardiolipin, Sphingosine-1-P." In A Guide to Phospholipid Chemistry. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780195079814.003.0009.

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In the previous chapters, the emphasis was placed on establishing the chemical nature of phospholipids normally found in relatively high concentrations in mammalian cells. The methodology described for identification of these compounds can be applied, perhaps with some minor modifications to the structural characterization of phospholipids found in plants, fish, and bacteria. Interwoven into the fabric of these chapters was the subtle reference to their potential biological role in cellular behavior. As lipid biochemistry has developed over the past several years, there is no doubt that the field of signal transduction has had an enormous impact on phospholipid awareness. As might be expected, the potential for phospholipids or their metabolites to exhibit biological activity loomed large. As will be evident in this chapter, phospholipids can certainly have biological activity and this theme shall be explored in some depth. The title “Minor Phospholipids” is not meant to be belittling, but is only intended to reflect the fact that these phospholipids are present in very low concentrations. In fact, some are considered to be formed only after a cell has been stimulated by an extracellular agonist. As shall be seen, these compounds have considerable biological activity and hence are really of major importance in the cellular metabolic scene. The term platelet activating factor (PAF) was originally applied to a phosphoglyceride capable of activating platelets, leading to their aggregation. In addition, in certain species, there was also discharge of their dense granules (as indicated by serotonin release from the platelets). This nomenclature was unfortunate because it is now well established that many cells can produce this compound and that, likewise, PAF can stimulate many other cells. There are many other compounds, such as thrombin and arachidonic acid, which also can activate platelets. Notwithstanding this problem of nomenclature, there is a widespread (deeply entrenched) usage of this term to indicate a specific type of phospholipid with a particular biological activity. Given the status of this field at the current time, the use of the term PAF will be continued here.

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Thompson, Philip, Neil Misso, Marion Passarelli, and Martin Phillips. "The Effect of Eicosapentaenoic Acid Consumption on Human Neutrophil Chemiluminescence." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch52.

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Webert, Kathryn E., and John G. Kelton. "Disorders of platelet number and function." In Oxford Textbook of Medicine. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.220603.

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Platelets are released from megakaryocytes in the bone marrow and circulate for 5 to 10 days before being cleared by the cells of the reticuloendothelial system. They play a critical role in haemostasis, with key features being (1) adhesion—when the wall of a blood vessel is damaged, platelets adhere to exposed collagen and other components of the subendothelium via the glycoprotein Ib receptor and other adhesive receptors; followed by (2) activation—release of thrombin, adenosine diphosphate, and arachidonic acid, which is converted by a cascade of enzymes into platelet activating agents including thromboxane A...

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Pollak, Eleanor S., and Katherine A. High. "Genetic disorders of coagulation." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0546.

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Haemophilia is a familial X-linked disorder due to deficiency of either factor VIII (haemophilia A) or factor IX (haemophilia B), components of the intrinsic enzymatic complex that activates factor X. Clinical features and diagnosis—the main manifestations are bleeding into joints and soft tissues, with haemophilic arthropathy and joint deformity being inevitable complications in untreated patients. Other features include pseudotumours, bleeding into the urinary system, and bleeding following clinical procedures. Laboratory diagnosis is based on a modification of the classic activated partial thromboplastin time (APTT) assay, with inhibitor screening used to exclude other causes of prolonged APTT. Treatment—involves the administration of the deficient factor VIII or factor IX, most commonly ‘on demand’ in response to bleeding, with prophylactic treatment given before surgery. Von Willebrand’s disease is a common autosomal dominant disorder of platelet function caused by a functional deficiency of von Willebrand factor (VWF). VWF, normally synthesized by megakaryocytes, prevents degradation of factor VIII; VWF, also made by endothelial cells, enhances platelet activation and recruitment at sites of tissue damage. Treatment—mild von Willebrand’s disease is treated with desmopressin 1-deamino-8-d-arginine vasopressin (DDAVP), which releases factor VIII and VWF from endothelial cells. Other treatments include ε‎-aminocaproic acid, oestrogens, and factor VIII concentrates. Other hereditary disorders of coagulation, including (1) hereditary deficiency of the plasma metalloproteinase ADAMTS13; (2) combined deficiency of coagulation factors V and VIII; (3) factor XI deficiency; (4) inherited deficiencies of factors II, V, VII, and X; and (5) deficiency of the contact activating factors, factor XIII, and fibrinogen, and hypercoagulable diseases due to deficiencies of anticoagulants or propensity to thrombosis are discussed in this chapter.

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Becker, Richard C., and Frederick A. Spencer. "Aggrenox and Cilostazol." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0015.

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The dipyridamole component of Aggrenox and cilostazol, both phosphodiesterase inhibitors, are used predominantly in patients with peripheral vascular and cerebrovascular disease. Aggrenox is a combination platelet antagonist that includes aspirin (25 mg) and dipyridamole (200 mg extended-release preparation). It is typically taken twice daily. Aspirin’s mechanism of action has been discussed previously. Dipyridamole inhibits cyclic adenosine monophosphate (cAMP)-phosphodiesterase (PDE) and cyclic-3´, 5´- guanylate monophospate (GMP)-PDE (Bunag et al., 1964). The pharmacokinetic profile of aspirin has been summarized previously. Peak dipyridamole levels in plasma are achieved within several hours of oral administration (400 mg dose of Aggrenox). Extensive metabolism via conjugation with glucuronic acid occurs in the liver. There are no significant pharmacokinetic interactions between aspirin and dipyridamole coadministered as Aggrenox. Dipyridamole inhibits platelet aggregation by two distinct mechanisms. First, it attenuates adenosine uptake into platelets (as well as endothelial cells and erythrocytes). The resulting increase elicits a rise in cellular adenylate cyclase concentrations, resulting in elevated cAMP levels, which inhibit platelet activation to several agonists, including adenosine diphosphate (ADP), collagen, and platelet-activating factor. Dipyridamole also inhibits PDE. The subsequent increase in cAMP elevates nitric oxide concentration, facilitating platelet inhibitory potential (Eisert, 2001). The European Stroke Prevention Study (ESPS)-2 reported that 79.9% of patients experienced at least one on-treatment adverse event. The most common side effects were gastrointestinal complaints and headache. Dipyridamole has vasodilatory effects and should be used with caution in patients with severe coronary artery disease in whom episodes of angina pectoris may increase. Patients receiving Aggrenox should not be given adenosine for myocardial perfusion studies. Plasma concentrations of dipyridamole are approximately 40% higher in patients greater than 65 years of age compared with younger individuals. Aggrenox has not been studied in patients with acute coronary syndrome (ACS). The ESPS-2 included 6,602 patients with ischemic stroke (76% of the total population) or transient ischemic attack who were randomized to receive Aggrenox, dipyridamole alone, aspirin alone, or placebo. Aggrenox reduced the risk of stroke by 22.1% compared with aspirin and by 24.4% compared with dipyridamole. Both differences were statistically significant (p = .008 and p = .002, respectively) (Diener et al., 1996).

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Conference papers on the topic "Platelet activating factor. Arachidonic acid"

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Del Maschio, A., M. Albors, F. Bucchi, et al. "HUMAN POLYMORPHONUCLEAR LEUKOCYTE ACTIVATION INDUCED BY PLATELET ACTIVATING FACTOR (PAF)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643482.

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Human polymorphonuclear leukocytes (PMNs) loaded with the photoprotein Aequorin, were exposed to PAF in the presence of extracellular Ca2+ (1 mM). PMNs aggregation measured In the “Platelet Ionized Calcium Aggregometer” (P.I.C.A.) was dependent on the concentration of the stimulus. Ca2+ cytoplasmatic increase was monitored in parallel at concentrations of PAF which did not modify cellular integrity (10-7-10-5M). The intracellular Ca2+ flux (up to 19±3 µM) triggered by PAF was also concentration-dependent. In order to establish the role played by this intracellular messenger, we studied some ce

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Bryckaert, M. C., A. Wasteson, G. Tobelem, F. Rendu, and J. P. Caen. "PLATELET DERIVED GROWTH FACTOR (PDGF) BINDS TO HUMAN PLATELETS AND MODULATES PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643493.

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PDGF which is released during platelet activation like the other ∝ granule components (fibrinogen, F VIII/vWF, PF4) could bind to platelet membrane Following this hypothesis, we have studied the binding of 125I pure human PDGF to washed human platelets activated by collagen. This binding was specific and time dependent and reached a plateau with 20 μg/ml of collagen. With 200 fold excess of unlabeled PDGF, the binding of 125I-PDGF decreased progressively to 10 .whereas unlabeled Epidermal Growth Factor did not compete with 125I-PDGF. Saturation curve and scatchard analysis have shown one class

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Bodzenta-Lukaszvk, A., K. Krupiński, and M. Bielawiec. "PLATELET FUNCTION AND KALLIKREIN SYSTEM IN PATIENTS WITH ESSENTIAL HYPERTENSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644258.

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Since the pathogenesis of hypertension is still discussed the aim of this study was to investigate behaviour of platelets and kallikrein system in patients suffering from this disease. In 30 patients with essential hypertension, aged 23-31 years and 20 normotensive healthy subjects, aged 21-35 years the following parameters of platelet function were studied: platelet aggregation induced with ADP,platelet activating factor (PAF) and arachidonic acid (AA) according Born's method, plasma beta-thromboglobulin (Beta-TG) and platelet factor 4 (PF4) , plasma thromboxane B2 (TXB2) and cyclic AMP using

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Chesney, C. M., and D. D. Pifer. "EFFECT OF Ca2+ and Mg2+ ON PLATELET ACTIVATING FACTOR (PAF) INDUCED AGGREGATION AND SPECIFIC BINDING TO HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642879.

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Gel filtered human platelets (GFP) collected in Tyrode's buffer containing 0.5 mM Ca+2, ImM Mg+2, and 0.35% albumin exhibit high affinity binding of 3H-PAF with a Kd of 0.109 α 0.029 nM (mean α SD; n=13) and 267 α 70 sites per platelet. When fibrinogen (1.67 mg/ml final concentration) is added to these GFP preparations biphasic aggregation is observed with PAF (4 nM). Normal aggregation is also observed with other platelet agonists including ADP, epinephrine, collagen, arachidonic acid, A23187 and thrombin. If GFP is prepared without added Ca+2 or Mg+2 in the presence of 3mM EDTA, platelets do

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Altman, R., A. Scazziota, S. Windor, and C. A. Dujovne. "ADDITIVE EFFECT OF DILTIAZEM (DIL) ON THE INHIBITION OF PLATELET AGGREGATION PRODUCED BY ASPIRIN (ASA)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643437.

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Platelet activation in vivo occurs by the action of several stimuli. It is generally agreed that actives products of arachidonic acid derived via the cyclooxy-genase pathway can stimulate platelet aggregation. ASA decrease thromboxane A2 generation and thereby inhibit platelet aggregation produced by AA and, partially, by others agonists. Nevertheless, the antiaggregating effect of ASA can be overcome by the conjointly activity of arachidonic acid(AA) and platelet activating factor (PAF). The inhibition of this cooperative aggregating effect can be important in platelet function suppressive th

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Gentry, P. A., and G. S. Bondy. "The aggregation of bovine platelets is not dependent on thromboxane B2 production." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644500.

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Bovine and human platelets appear to be equally sensitive to inhibition by several environmental toxins even though the bovine is not generally recognised as a species prone to thromboembolic and hemorrhagic disease. During the examination of the mechanism of action of the toxins it became necessary to establish parameters for normal bovine platelet function.Bovine platelets suspended in homologous plasma demonstrate various responses to different agonists. Bovine platelets aggregate effectively and irreversibly to fibrillar form collagen and adenosine-diphosphate (ADP), undergo reversible agg

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Mointire, V. L., A. J. Frangos, G. B. Rhee, G. S. Eskin, and R. E. Hall. "RHEOLOGY AND CELL ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643988.

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The subject of this work is to examine the hypothesis that some sublytic levels of mechanical perturbation of cells can stimulate cell metabolism. As a marker metabolite, we have chosen arachidonic acid. Principal metabolites for platelets include the cyclooxygenase product thromboxane A2(TXA2) and the lipoxygenase product 12-hydroperoxy-eicosatetraenoic acid (12-HPETE). Polymorphonuclear leukocytes (PMNLs) initally produce principally 5-HPETE, somtimes leading to the formation leukotrienes, though many other metabolites of arachidonic acid have been isolated from activated neutrophils. Human

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Wyler, B., and K. J. Clemetson. "THE ROLE OF GPIb IN PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642922.

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Platelet membrane glycoprotein lb (GPIb) is known to contain a receptor for von Willebrand factor (vWf) and for thrombin. The role of GPIb in platelet activation was investigated by comparing the effect of removal of the binding sites by specific proteolysis with that of blocking them using specific antibodies. Specific removal of the 45 kDa outer part of GPIb by treatment of platelets with human leukocyte elastase caused loss of platelet agglutination response to von Willebrand factor (vWf) but also a weaker activation by thrombin similar to that found with Bernard-Soulier syndrome platelets

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Voss, R., H. D. Ohanes, H. Ditter, and F. R. Matthias. "REFRACTORINESS OF PLATELETS AFTER REVERSIBLE STIMULATION BY ADP, PAF AND AA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644547.

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It has been observed that platelets which have been, stimulated by thrombin, ADP or platelet-activating factor (PAF) show an inhibited response to a subsequent stimulation by the same agonist. We performed a crossover stimulation of human platelets (PRP) with the four agonists ADP, PAF, arachidonic acid(AA) and collagen (COL); after a first stimulation with a dose giving a reversible aggregation (0,1-0,4×10-6M ADP, 0,1-0,5×10-8 M PAF) or a shape change (0,05-0, 1mM AA., 0,4 ug/ml COL) the platelets were again stimulated after 5 min with the same or a higher dose, usuallyresulting in an irK8 re

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Montecchio, G. P., P. Custodi, S. Carbone, C. Bendotti, and F. Piovella. "TICLOPIDINE AND INDOBUFEN: EFFECTS ON HAEMOSTATIC FUNCTIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643418.

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Many different mechanisms are involved in thrombus formation. We compared the effects on haemostatic function of two drugs having different mechanism of action, the one interfering with arachidonic acid metabolic cascade (Indobufen) and the other (Ticlopidine) independent from it. 18 adult patients of both sexes suffering from cerebral Transient Ischaemic Attack (T.I.A.) or Reversible Ischaemic Neurologic Disability (R.I.N.D.) have been treated with Indobufen (400 mg daily) or Ticlopidine (500 mg daily) for three weeks. The effects on various haemostatic parameters including bleeding time, pla

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