Gotowe bibliografie tematyczne / Vascular-platelet mechanism

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Gotowa bibliografia na temat „Vascular-platelet mechanism”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Vascular-platelet mechanism"

Freedman, Jane. "Toll-Like Receptors: Mechanism and Relation to Human Populations." Blood 128, no. 22 (2016): SCI—46—SCI—46. http://dx.doi.org/10.1182/blood.v128.22.sci-46.sci-46.

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Abstract Inflammation and infection are known to alter platelet count, production, and function and major studies have demonstrated that acute infection is associated with a transient 5-fold increased risk of thrombotic vascular syndromes including stroke, acute myocardial infarction, and peripheral vascular occlusion. Platelets play an intricate role in thrombosis, myocardial infarction, and thrombotic stroke and are now being appreciated for their functional innate immune receptors. More recently, platelets have been connected to the host's immune system via their ability to trap bacteria an

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Cohen, RA. "Platelet 5-Hydroxytryptamine and Vascular Adrenergic Nerves." Physiology 3, no. 5 (1988): 185–89. http://dx.doi.org/10.1152/physiologyonline.1988.3.5.185.

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Platelets contain and release large amounts of 5-hydroxytryptamine that can influence the function of vascular adrenergic nerves. The immediate effect on neuronal function of low concentrations of the amine is to inhibit norepinephrine release. 5-Hydroxytryptamine may also be accumulated by the same uptake mechanism that reaccumulates norepinephrine into the adrenergic nerve endings. In diseased blood vessels where platelet aggregation occurs, 5-hydroxytryptamine may therby assume an alternative transmitter role, altering the function of the sympathetic nerves.

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Nightingale, Angus K., Philip P. James, Jayne Morris-Thurgood, et al. "Evidence against oxidative stress as mechanism of endothelial dysfunction in methionine loading model." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 3 (2001): H1334—H1339. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1334.

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Endothelial dysfunction reflects reduced nitric oxide (NO) bioavailability due to either reduced production, inactivation of NO, or reduced smooth muscle responsiveness. Oral methionine loading causes acute endothelial dysfunction in healthy subjects and provides a model in which to study mechanisms. Endothelial function was assessed using flow-mediated dilatation (FMD) of the brachial artery in humans. Three markers of oxidative stress were measured ex vivo in venous blood. NO responsiveness was assessed in vascular smooth muscle and platelets. Oral methionine loading induced endothelial dysf

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Nesbitt, Warwick S., Simon Giuliano, Suhasini Kulkarni, Sacha M. Dopheide, Ian S. Harper, and Shaun P. Jackson. "Intercellular calcium communication regulates platelet aggregation and thrombus growth." Journal of Cell Biology 160, no. 7 (2003): 1151–61. http://dx.doi.org/10.1083/jcb.200207119.

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The ability of platelets to form stable adhesion contacts with other activated platelets (platelet cohesion or aggregation) at sites of vascular injury is essential for hemostasis and thrombosis. In this study, we have examined the mechanisms regulating cytosolic calcium flux during the development of platelet–platelet adhesion contacts under the influence of flow. An examination of platelet calcium flux during platelet aggregate formation in vitro demonstrated a key role for intercellular calcium communication (ICC) in regulating the recruitment of translocating platelets into developing aggr

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Mezger, M., K. Göbel, P. Kraft, S. G. Meuth, C. Kleinschnitz, and H. F. Langer. "Platelets and vascular inflammation of the brain." Hämostaseologie 35, no. 03 (2015): 244–51. http://dx.doi.org/10.5482/hamo-14-11-0071.

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SummaryThere is emerging evidence that platelets have an important role in inflammation beyond their involvement in hemostasis. Platelets can contribute to inflammatory reactions via crosstalk both with immune cells and endothelial cells. Inflamed vessels are characterized by the presence of activated endothelial cells. These activated endothelial cells upregulate receptors necessary for leukocyte recruitment, but also for the adhesion of platelets. Subsequently, immune cells can bind to platelets through adhesion receptors presented on the platelet surface, thus supporting leukocyte recruitme

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Gong, Shengyang, and Zheng Cao. "Research Progress on the Anti-Atherosclerotic Effect and Mechanism of Tetramethylpyrazine." Journal of Clinical and Nursing Research 8, no. 6 (2024): 94–99. http://dx.doi.org/10.26689/jcnr.v8i6.7032.

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Atherosclerosis is a chronic vascular disease and the most common pathological change of cardiovascular disease. Its pathogenesis is closely related to inflammation, oxidative stress, lipid accumulation, and calcinosis. Tetramethylpyrazine plays an anti-atherosclerotic role by regulating lipid metabolism, inhibiting foam cell formation, alleviating inflammation, inhibiting vascular calcification and abnormal platelet activation, and has a cardiovascular protective effect. Therefore, this paper summarized the research progress of the anti-atherosclerosis effect and mechanism of tetramethylpyraz

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Meng, Qingyu, Xichun Li, Mingyu Zhao, Shusen Lin, Xiangwen Yu та Guanglong Dong. "Study on the Mechanism of Platelet-Released Clusterins Inducing Restenosis after Carotid Endarterectomy by Activating TLR3/NF-κb p65 Signaling Pathway". Journal of Healthcare Engineering 2022 (10 січня 2022): 1–8. http://dx.doi.org/10.1155/2022/7631126.

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This study aimed to explore the role of clusterin released by platelet aggregation in restenosis after carotid endarterectomy. 35 patients who underwent carotid endarterectomy due to carotid artery stenosis were enrolled in this study. They were admitted to the Third Affiliated Hospital of Qiqihar Medical University from January 2018 to January 2019. All the patients were divided into two groups: the restenosis group and the nonrestenosis group, according to the follow-up results within 12 months. Peripheral blood was collected on the first day, 6 months, and 12 months after operation. The exp

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Gavrilovskaya, Irina N., Elena E. Gorbunova, and Erich R. Mackow. "Pathogenic Hantaviruses Direct the Adherence of Quiescent Platelets to Infected Endothelial Cells." Journal of Virology 84, no. 9 (2010): 4832–39. http://dx.doi.org/10.1128/jvi.02405-09.

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ABSTRACT Hantavirus infections are noted for their ability to infect endothelial cells, cause acute thrombocytopenia, and trigger 2 vascular-permeability-based diseases. However, hantavirus infections are not lytic, and the mechanisms by which hantaviruses cause capillary permeability and thrombocytopenia are only partially understood. The role of β3 integrins in hemostasis and the inactivation of β3 integrin receptors by pathogenic hantaviruses suggest the involvement of hantaviruses in altered platelet and endothelial cell functions that regulate permeability. Here, we determined that pathog

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Mousa, Shaker, and Joel Bennett. "Platelet Function Inhibitors in the Year 2000." Thrombosis and Haemostasis 85, no. 03 (2001): 395–400. http://dx.doi.org/10.1055/s-0037-1615595.

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SummaryPlatelet thrombi are responsible for much of the morbidity and mortality of arterial vascular disease (1). Because platelet inhibitors such as aspirin have proven to be of benefit to patients with these disorders, there has been a directed search for more potent anti-platelet agents. The following discussion addresses the mechanism of action and clinical utility of the currently available platelet function inhibitors. Although in theory these agents could impair platelet adhesion, aggregation, secretion, or platelet procoagulant activity, in practice they are focused almost exclusively

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Markmeyer, Paulina, Franziska Lochmann, Kunal Kumar Singh, et al. "Procoagulant Extracellular Vesicles Alter Trophoblast Differentiation in Mice by a Thrombo-Inflammatory Mechanism." International Journal of Molecular Sciences 22, no. 18 (2021): 9873. http://dx.doi.org/10.3390/ijms22189873.

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Procoagulant extracellular vesicles (EV) and platelet activation have been associated with gestational vascular complications. EV-induced platelet-mediated placental inflammasome activation has been shown to cause preeclampsia-like symptoms in mice. However, the effect of EV-mediated placental thrombo-inflammation on trophoblast differentiation remains unknown. Here, we identify that the EV-induced thrombo-inflammatory pathway modulates trophoblast morphology and differentiation. EVs and platelets reduce syncytiotrophoblast differentiation while increasing giant trophoblast and spongiotrophobl

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Rozprawy doktorskie na temat "Vascular-platelet mechanism"

Liu, Yanxia Medical Sciences Faculty of Medicine UNSW. "Mechanisms regulating platelet-derived growth factor-D transcription in vascular smooth muscle cells." Awarded by:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/43372.

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Platelet-derived growth factor D-chain (PDGF-D) is the newest member of the PDGF family of mitogens and chemo-attractants; it is expressed in a wide variety of cell types, including vascular smooth muscle cells (SMCs). The molecular mechanisms regulating PDGF-D transcription are unknown. Here I investigated the effects of angiotensin II (ATIl) and IL-1 beta on the transcription of PDGF-D and changes in vascular SMCs phenotype. Primer extension analysis mapped a single transcriptional start site to the ccAG CGC motif of PDGF-D promoter. Several potential transcription factor binding sites such

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Lo, I.-Chung, and 羅翊中. "Molecular Mechanisms for Platelet-derived Growth Factor-BB-induced Thrombomodulin Expression in Human Vascular Smooth Muscle Cells." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/83501690361216860596.

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博士<br>國立成功大學<br>基礎醫學研究所<br>97<br>Thrombomodulin (TM), a potent anticoagulant, is not expressed in quiescent vascular smooth muscle cells (VSMCs). During vascular remodeling, TM is expressed in VSMCs but the regulatory mechanisms remain unclear. This study examined molecular mechanisms for TM expression in VSMCs. Platelet-derived growth factor-BB (PDGF-BB) treatment upregulated TM protein levels by 7.5- fold in time- and dosage-dependent manner in cultured human aortic VSMCs. PDGF-induced TM is functional in activating protein C. In isolated endothelium-denuded aortae, TM expression was stimula

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Książki na temat "Vascular-platelet mechanism"

Wijdicks, Eelco F. M., and Sarah L. Clark. Antiplatelet Agents. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0009.

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Antiplatelet agents are commonly used in vascular medicine and cardiology, but also in the pharmacologic management of patients with ischemic stroke. Aspirin alone remains the mainstay of therapy for secondary stroke prevention. Several landmark studies for the optimal duration and dose of antiplatelet therapy in stroke prevention are discussed. Dual antiplatelet therapy is needed after carotid artery stenting. Situations where antiplatelet agents also come into play are endovascular procedures associated with procedure-related thrombi. Antiplatelet agents have different mechanisms of action,

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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across

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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and

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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and

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Części książek na temat "Vascular-platelet mechanism"

Imada, Keisuke, Yu Hosokawa, Masaharu Terashima, et al. "Inhibitory Mechanism of Taurine on the Platelet-Derived Growth Factor BB-Mediated Proliferation in Aortic Vascular Smooth Muscle Cells." In Advances in Experimental Medicine and Biology. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0077-3_2.

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Buring, Julie E., and Charles H. Hennekens. "Aspirin." In Prevention of Myocardial Infarction. Oxford University PressNew York, NY, 1996. http://dx.doi.org/10.1093/oso/9780195085822.003.0012.

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Abstract In the fifth century B.C., Hippocrates discovered that an extract of willow bark had analgesic properties. The pain-killing effect was the result of salicin, a naturally occurring chemical in willow bark, which is closely related to today’s synthetic aspirin, acetylsalicylic acid. It is only quite recently, however—over the past few decades—that attention has focused on the potential role of aspirin in reducing risks of occlusive vascular disease. The hypothesized mechanism for aspirin’s benefit is its ability to decrease platelet aggregation and thereby reduce the risk of thrombotic

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Briones-Aranda, Alfredo, Josselin Corzo-Gómez, Diana Casique-Aguirre, and Mauricio Megchún-Hernández. "The platelet serotonergic system and the search for new biomarkers and therapeutic options for diverse diseases." In Serotonin - Neurotransmitter and Hormone of Brain, Bowels and Blood [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.1003630.

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The latest advances in basic and clinical research on the main components of the platelet serotonergic system are presently reviewed. These components consist of serotonin (5-HT), enzymes that participate in 5-HT metabolism, the serotonin transporter (SERT), and 5-HT1A, 5-HT2A, 5-HT3, and 5-HT4 receptors (each with their corresponding mechanism of intracellular transduction). An additional focus is on related biomarkers or drugs for the diagnosis or treatment of the pathophysiology of diverse disorders such as depression, anxiety, hemorrhagic dengue, coagulopathy generated by COVID-19, myocard

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Becker, Richard C., and Frederick A. Spencer. "Novel Platelet Antagonists." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0016.

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The development of pharmacologic agents that inhibit platelet performance could not have proceeded without a fundamental knowledge of normal biology and a clear understanding of the laws that govern cellular events in the circulatory system. The adhesion of platelets to a site of vessel wall injury is mediated by von Willebrand factor (vWF), which binds to the platelet glycoprotein (GP) Ib/IX-V complex receptor (and the GPIIb/IIIa receptor under high shear stress conditions). Monoclonal antibodies to vWF have been developed and tested in animal models, as has aurintricarboxylic acid (Strony et

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Bahou, Wadie F. "Disorders of Platelets." In Genomics and Clinical Medicine. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195188134.003.0015.

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Abstract Overview of Platelet Biology and Function Blood coagulation is controlled by a tightly regulated cascade of proteases and their cofactors that sequentially lead to the generation of a gelatinous meshwork of protein called fibrin. This coagulation mechanism ensures the normal cessation of blood flow that occurs during physiological processes such as wounding or menstruation, and is termed hemostasis. Human blood platelets play a critical function in the maintenance of primary hemostasis, not only via adhesive interactions with the sub endothelial matrix but also by providing the negati

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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 aspi

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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 selective

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Wu, Chieh-Hsi, Chun-Hsu Pan, and Ming-Jyh Sheu. "Therapeutic Applications and Mechanisms of YC-1: A Soluble Guanylate Cyclase Stimulator." In Vascular Biology - Selection of Mechanisms and Clinical Applications. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.84572.

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Nitric oxide (NO) is an essential endogenous vasodilator to maintain vascular homeostasis, whose effects are mainly mediated by NO-dependent soluble guanylate cyclase (sGC) which catalyzes the synthesis of cyclic guanosine monophosphate (cGMP), a critical mediator of vascular relaxation. YC-1, a novel NO-independent sGC stimulator, was first introduced as an inhibitor of platelet aggregation and thrombosis. Accumulating studies revealed that YC-1 has multiple medication potentials to use for a broad spectrum of diseases ranging from cardiovascular diseases to cancers. In contrast to NO donors,

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Pasquali, Christian, Daniel Zingg, Stefania Ballarini, Giovanni A. Rossi, and Hermann Haller. "The Place of Mature Drugs in COVID-19 Era." In Frontiers in Clinical Drug Research-Anti Infectives Volumee 9. BENTHAM SCIENCE PUBLISHERS, 2024. http://dx.doi.org/10.2174/9789815179811123090003.

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COVID-19 infection, caused by the SARS-CoV-2 virus, is associated with substantial morbidity and mortality. COVID-19 infection has three distinct phases: 1, early infection phase; 2, pulmonary phase; and 3, the hyperinflammatory phase. Despite a major focus on vaccines and new therapeutics, existing drugs sharing some known mechanistic with this virus, have also gained interest. The potential positioning of three mature innovative drugs, which could be of potential use in this pandemic environment, is discussed in this chapter: OM-85 and calcium dobesilate, and their salt form etamsylate, have

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Mankiewicz, Kimberly A., and Leonard K. Seibold. "Wound Healing In Glaucoma." In Complications of Glaucoma Surgery. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780195382365.003.0013.

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The goal of wound healing in most surgeries is to bring the injured tissue back to its original state to prevent the wound from reopening. However, in glaucoma surgery, the goal is to have incomplete wound healing. Scar formation prevents the filtering mechanism and bleb from functioning properly, leading to poor pressure control and failure of the surgery. However, if there is too little wound healing, surgical failure may be marked by overfiltration and hypotony. Several modulators are currently used in conjunction with glaucoma surgery, and new targets are under investigation to improve our

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Streszczenia konferencji na temat "Vascular-platelet mechanism"

Rieg, Annette D., Carolin Anker, Julia Krabbe, Rolf Rossaint, Stefan Uhlig, and Christian Martin. "Dual mechanism of platelet-derived growth factor (PDGF)-receptor: Contribution of vascular response to the pathogenesis of pulmonary hypertension (PH)." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2437.

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Johnson, G. J., P. C. Dunlop, M. J. Rabiet, L. A. Leis, and AH L. From. "THE DIHYDROPYRIDINE CALCIUM CHANNEL AGONIST, BAY K 8644, AND THE ANTAGONIST, NIFEDIPINE, INHIBIT U46619-INDUCED HUMAN PLATELET ACTIVATION BY COMPETITIVE BINDING TO THE THROMBOXANE A22/PGH2 RECEPTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643756.

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The dihydropyridine (DP) Ca2+ channel antagonist, nifedipine (NF), inhibits platelet aggregation .in vitro and ex vivo by an undefined mechanism. Inhibition of Ca2+ influx via Ca2+ channels is a postulated mechanism, but voltage-dependent Ca2+ channels have not been demonstrated in platelets. We previously observed that NF blocked thromboxane A2 (TXA2)-induced platelet aggregation and secretion. In order to further evaluate the mechanism of DP inhibition of platelet activation, we studied the effects of NF and BAY K 8644, (BAY), a DP with opposite (agonist) effects on muscle cells, on human pl

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Stuart, M. J., P. D. Sadowitz, and B. N. Y. Setty. "PLATELET 12-HYDROXY-5,8,10-HEPTADECATRIENOIC ACID (HHT) STIMULATES PROSTACYCLIN PRODUCTION BY ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642836.

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Although HHT accounts for approximately one third of the ara-chidonic acid (AA) metabolites produced by stimulated platelets, no well defined function has been attributed to this platelet product. We report that HHT stimulates prostacyclin production by endothelial cells, and have identified the mechanism for this effect. In human umbilical venous endothelial cells HHT (0.5 and 1pM) stimulated prostacyclin (RIA for 6KPGF1α) by 32±10% (1 SE) and 42±13% (P<0.05 and (0.01). Similar changes were observed when the effect of HHT on exogenous [1 -14C] AA metabolism in fetal bovine aortic endotheli

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Janssens, W. J., and J. M. Van Nueten. "VASOCONSTRICTOR EFFECTS OF AGGREGATING PLATELETS IN RABBIT PULMONARY ARTERIES WITH AND WITHOUT ENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643354.

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The aim of the present experiments was to investigate the modulatory role of the endothelium on vasoconstrictions induced by aggregating platelets. Rings of rabbit pulmonary arteries were mounted for isometric tension recording. The presence or absence of the endothelium was confirmed using acetylcholine-induced relaxations. All contractions were expressed as percentage of a K+-induced (100 mM) contraction. Thrombin was administered to the preparations at 0.5 NIH units/ml. At this concentration the enzyme caused no or only very small contractions, but apparently induced maximal platelet activa

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Chamone, D. A. F., A. Y. Hoshikawa-Fujimura, C. Massumoto, G. Bellotti, F. Arashiro, and M. Jamra. "ABNORMALITIES OF PLATELET AGGREGATION AND ENHANCED FACTOR X ACTIVATOR ACTIVITY OF WASHED PLATELETS IN SICKLE CELL DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644544.

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The occurence of microvascular occlusion is one of the most prominent pathologic features of sickle cell anemia. The mechanism of vaso occlusion has generally been attributed to the abnormal shape and reduced deformability of the sickled erithrocy tes. However, the involvement of vascular endothelium, platelets and their interactions with coagulation factors may also be of pathogenic significance in microvascular occlusive crises.We investigated the interaction between vascular endothelium, platelets and blood coagulation factors in 23 patients with Sickle Cell Disease (SCD) and in normal volu

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patrono, C. A. "CLINICAL TRIALS OF ANTITHROMBOTIC AGENTS IN UNSTABLE ANGINA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643713.

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A Veterans Administration (VA) Cooperative Study (NEJM 309:396,1983) has demonstrated that a single daily administration of aspirin 324 mg in buffered solution, started within 51 hours of admission to the hospital, significantly reduced the 12-week incidence of acute myocardial infarction (MI) or death by 51% in men with unstable angina. These results have been substantially confirmed by a Canadian Multicenter Trial (NEJM 313:1369,1985) in patients of both sexes treated with aspirin 325 mg qid. The rate of death or acute MI wasfound to be 51% lower in the group treated with aspirin,after a mea

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Catalano, M., S. Belletti, E. Coazzoli, et al. "TREATMENT OF PERIPHERAL VASCULAR DISEASE WITH ILOPROST (ZK36374)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644822.

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The action of a stable analogue of prostacyclin, Iloprost, was studied in 18 male in-patients aged 51-69 yr (mean 61±7) with peripheral vascular disease Fontaine stage lib and III who gave informed consent. Entry criteria were Fontaine stage III or II with free interval at treadmill test ≺ 100 m. (4 km/h, without slope), ankle/arm arterial pressure index (API)≺0.7 at rest. Patients with arterial hypertension, diabetes, myocardial infarction in the previous 6 mo, heart failure, thrombocytopenia, hemorrhagic diathesis, or kidney or liver failure were excluded. The patients underwent 3 weeks' tre

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Bowen-Pope, D. F., C. Gajdusek, J. Harlan, et al. "REGULATION OF GROWTH FACTOR PRODUCTION BY ENDOTHELIAL CELLS IN RESPONSE TO COAGULATION AND INFLAMATORY FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642947.

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Platelet-derived growth factor (PDGF) is a polypeptide growth factor first discovered in, and purified from, human blood platelets. As assayed by its ability to stimulate proliferation of cultured vascular smooth muscle cells, PDGF is the major mitogen in human whole blood serum. PDGF has also been reported to be chemotactic for fibroblasts, vascular smooth muscle cells, and leukocytes, and to be able to stimulate contraction of arterial smooth muscle. This, spectrum of activities suggests that PDGF could play a significant role in several vascular processes, including wound repair and the for

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Violi, F., C. Cimminiello, S. Chierichetti, M. Scatigna, P. Rizzon, and F. Balsano. "STAI (Studio Ticlopidina Angina Instabile) PROJECT. TICLOPIDINE -IN UNSTABLE ANGINA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644818.

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The treatment of patients suffering from unstable angina (UA) with antiplatelet drugs is a therapeutic approach that provided interesting results.Patients given aspirin, that inhibits cyclooxigenase pathway (CP) showed a significant reduction of cardiovascularevents.Quite surprisingly sulfinpirazone, that possesses a mechanism of action similar to aspirin, did not influence cardiovascular complications of UA patients.To further investigate the role of platelets in UA patients, we planned to study if ticlopidine (T), that inhibits platelet function by blocking fibrinogen binding to platelets, i

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Prosdocimi, M., M. Finesso, and A. Zatta. "A DOG MODEL OF PERIPHERAL ARTERIAL THROMBOSIS: POSSIBLE PHARMACOLOGICAL CONTROL OF VASCULAR OCCLUSION IN A STENOTIZED FEMORAL ARTERY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643185.

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It has been described by several authors that a critical stenosis of a dog coronary artery causes cyclical blood flow variations (CBFV), which are caused by platelet plugging of the vessel. Little information is available on the mechanism of thrombus formation in a stenotized peripheral artery and on the pharmacological control of this phenomenon. Male beagle dogs were anesthetized with sodium pentobarbital, artificially ventilated and prepared for the recording of arterial pressure, heart rate and femoral blood flow. A cylinder of Lexan with internal diameter of 1.6-1.8 mm and a length of 2.0

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