Relevant bibliographies by topics / Microthrombi

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

Academic literature on the topic 'Microthrombi'

Author: Grafiati
Published: 21 December 2024

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Journal articles on the topic "Microthrombi"

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Olson, Timothy M., David J. Driscoll, William D. Edwards, Francisco J. Puga, and Gordon K. Danielson. "Pulmonary microthrombi." Journal of Thoracic and Cardiovascular Surgery 106, no. 4 (October 1993): 739–44. http://dx.doi.org/10.1016/s0022-5223(19)33719-5.

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Fitzpatrick, James E., Carl Johnson, M. C. Major, Paul Simon, James Owenby, and Lieutenant Colonel. "Cutaneous Microthrombi." American Journal of Dermatopathology 9, no. 5 (October 1987): 419–22. http://dx.doi.org/10.1097/00000372-198710000-00008.

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Mihalko, Emily P., Megan Sandry, Nicholas Mininni, Kimberly Nellenbach, Halston Deal, Michael Daniele, Kamrouz Ghadimi, Jerrold H. Levy, and Ashley C. Brown. "Fibrin-modulating nanogels for treatment of disseminated intravascular coagulation." Blood Advances 5, no. 3 (January 29, 2021): 613–27. http://dx.doi.org/10.1182/bloodadvances.2020003046.

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Abstract Disseminated intravascular coagulation (DIC) is a pathological coagulopathy associated with infection that increases mortality. In DIC, excessive thrombin generation causes symptoms from formation of microthrombi to multiorgan failure; bleeding risks can also be a concern because of clotting factor consumption. Different clinical events lead to DIC, including sepsis, trauma, and shock. Treatments for thrombotic episodes or bleeding presentation in DIC oppose each other, thus creating therapeutic dilemmas in management. The objective of this study was to develop fibrin-specific core-shell nanogels (FSNs) loaded with tissue-type plasminogen activator (tPA) to treat the microcirculatory complications of DIC, which would facilitate targeted clot dissolution to manage microthrombi and the potential consumptive coagulopathy that causes bleeding. FSNs enhance formation of actively polymerizing clots by crosslinking fibrin fibers, but they can also target preexisting microthrombi and, when loaded with tPA, facilitate targeted delivery to lyse the microthrombi. We hypothesized that this dual action would simultaneously address bleeding and microthrombi with DIC to improve outcomes. In vivo, tPA-FSNs decreased the presentation of multiorgan microthrombi, recovered platelet counts, and improved bleeding outcomes in a DIC rodent model. When incorporated with human DIC patient plasma, tPA-FSNs restored clot structure and clot growth under flow. Together, these data demonstrate that a fibrinolytic agent loaded into fibrin-targeting nanogels could improve DIC outcomes.
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Shao, Bojing, Mark G. Wahrenbrock, Longbiao Yao, Tovo David, Shaun R. Coughlin, Lijun Xia, Ajit Varki, and Rodger P. McEver. "Carcinoma mucins trigger reciprocal activation of platelets and neutrophils in a murine model of Trousseau syndrome." Blood 118, no. 15 (October 13, 2011): 4015–23. http://dx.doi.org/10.1182/blood-2011-07-368514.

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Abstract Trousseau syndrome is classically defined as migratory, heparin-sensitive but warfarin-resistant microthrombi in patients with occult, mucinous adenocarcinomas. Injecting carcinoma mucins into mice generates platelet-rich microthrombi dependent on P- and L-selectin but not thrombin. Heparin prevents mucin binding to P- and L-selectin and mucin-induced microthrombi. This model of Trousseau syndrome explains resistance to warfarin, which inhibits fluid-phase coagulation but not selectins. Here we found that carcinoma mucins do not generate microthrombi in mice lacking P-selectin glycoprotein ligand-1 (PSGL-1), the leukocyte ligand for P- and L-selectin. Furthermore, mucins did not activate platelets in blood from PSGL-1–deficient mice. Mucins induced microthrombi in radiation chimeras lacking endothelial P-selectin but not in chimeras lacking platelet P-selectin. Mucins caused leukocytes to release cathepsin G, but only if platelets were present. Mucins failed to generate microthrombi in cathepsin G-deficient mice. Mucins did not activate platelets in blood from mice lacking cathepsin G or protease-activated receptor-4 (PAR4), indicating that cathepsin G activates platelets through PAR4. Using knockout mice and blocking antibodies, we found that mucin-triggered cathepsin G release requires L-selectin and PSGL-1 on neutrophils, P-selectin on platelets, and Src family kinases in both cell types. Thus, carcinoma mucins promote thrombosis through adhesion-dependent, bidirectional signaling in neutrophils and platelets.
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Park, Sohyung, and Byung-Ha Choi. "Acute Myocardial Infarction with Microthrombi in Cardiac Small Vessels after COVID-19 Vaccination (ChAdOx1 nCov-19): A Case Report." Korean Journal of Legal Medicine 45, no. 4 (November 30, 2021): 127–32. http://dx.doi.org/10.7580/kjlm.2021.45.4.127.

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We present the postmortem findings of an unexpected death due to acute myocardial infarction (AMI) with microthrombi and thrombosis in other vessels after the first dose of coronavirus disease 2019 (COVID-19) vaccination (ChAdOx1 nCov-19). The deceased was a 69-year-old woman who complained of nonspecific symptoms shortly after vaccination and was found dead on the sixth day. Postmortem examination revealed AMI and complications (left ventricular rupture, hemopericardium) with microthrombi in small cardiac vessels, which are similar to the characteristic findings of myocardial injury caused by microthrombi in patients with COVID-19. Nonobstructive thromboembolism in the pulmonary arteries and inferior vena cava, and fibrin microthrombi in some small vessels in the brain were also observed. It is unclear whether these findings are associated with COVID-19 vaccination, and further comprehensive studies are needed.
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Neil, Desley A. H. "CD31 highlights platelet-rich microthrombi." Histopathology 54, no. 3 (February 2009): 387–88. http://dx.doi.org/10.1111/j.1365-2559.2008.03215.x.

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Dienel, Ari, Remya Ammassam Veettil, Sung-Ha Hong, Kanako Matsumura, Peeyush Kumar T., Yuanqing Yan, Spiros L. Blackburn, et al. "Microthrombi Correlates With Infarction and Delayed Neurological Deficits After Subarachnoid Hemorrhage in Mice." Stroke 51, no. 7 (July 2020): 2249–54. http://dx.doi.org/10.1161/strokeaha.120.029753.

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Background and Purpose: Delayed neurological deficits are a devastating consequence of subarachnoid hemorrhage (SAH), which affects about 30% of surviving patients. Although a very serious concern, delayed deficits are understudied in experimental SAH models; it is not known whether rodents recapitulate the delayed clinical decline seen in SAH patients. We hypothesized that mice with SAH develop delayed functional deficits and that microthrombi and infarction correlate with delayed decline. Methods: Adult C57BL/6J mice of both sexes were subjected to endovascular perforation to induce SAH. Mice were allowed to survive for up to 1 week post-ictus and behavioral performance was assessed daily. Postmortem microthrombi, large artery diameters (to assess vasospasm), and infarct volume were measured. These measures were analyzed for differences between SAH mice that developed delayed deficits and SAH mice that did not get delayed deficits. Correlation analyses were performed to identify which measures correlated with delayed neurological deficits, sex, and infarction. Results: Twenty-three percent of males and 47% of females developed delayed deficits 3 to 6 days post-SAH. Female mice subjected to SAH had a significantly higher incidence of delayed deficits than male mice with SAH. Mice that developed delayed deficits had significantly more microthrombi and larger infarct volumes than SAH mice that did not get delayed deficits. Microthrombi positively correlated with infarct volume, and both microthrombi and infarction correlated with delayed functional deficits. Vasospasm did not correlate with either infarction delayed functional deficits. Conclusions: We discovered that delayed functional deficits occur in mice following SAH. Sex differences were seen in the prevalence of delayed deficits. The mechanism by which microthrombi cause delayed deficits may be via formation of infarcts.
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Redfern, Andrew, Huda Mahmoud, Tom McCulloch, Adam Shardlow, Matthew Hall, Catherine Byrne, and Nicholas M. Selby. "Renal Arcuate Vein Microthrombi-Associated AKI." Clinical Journal of the American Society of Nephrology 10, no. 2 (December 1, 2014): 180–86. http://dx.doi.org/10.2215/cjn.01540214.

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Skjørten, Fredrik. "ON THE NATURE OF HYALINE MICROTHROMBI." Acta Pathologica Microbiologica Scandinavica 73, no. 4 (August 17, 2009): 489–501. http://dx.doi.org/10.1111/j.1699-0463.1968.tb03208.x.

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Skjørten, Fredrik. "HYALINE MICROTHROMBI IN AN AUTOPSY MATERIAL." Acta Pathologica Microbiologica Scandinavica 76, no. 3 (August 18, 2009): 361–75. http://dx.doi.org/10.1111/j.1699-0463.1969.tb03267.x.

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Dissertations / Theses on the topic "Microthrombi"

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Picot, Audrey. "Develοpment οf a theranοstic agent fοr micrοthrοmbοsis during ischemic strοke." Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMC418.

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De nouvelles études suggèrent que l'accident vasculaire cérébral ischémique est fréquemment associé à la formation de microthrombi dans la microcirculation corticale. Ces microthrombi sont associés à une augmentation de la taille de la lésion, à un déclin cognitif et à la démence. Il est difficile de prendre en charge ces microthrombi car les méthodes d'imagerie actuelles ne permettent pas de les détecter. Pour y remédier, un nouvel agent théranostique a été développé, les IO@PDA@tPA, combinant des microparticules d'oxyde de fer (IO) enrobées de polydopamine (PDA) et conjuguées avec l’activateur tissulaire du plasminogène (r-tPA). Ce nouvel agent a montré son efficacité in vitro, non seulement sur la lyse de caillots, mais également sur les espèces réactives de l'oxygène qui sont significativement moins exprimées par les neurones soumis à une privation d'oxygène et de glucose. In vivo, l'administration des IO@PDA@tPA à un quart de la dose standard de r-tPA a permis la visualisation et la dégradation des microthrombi, détectées par imagerie par résonance magnétique (IRM) pondérée en T2*. Ce traitement a réduit de manière significative la taille de la lésion et favorisé la recanalisation 24 heures après le début de l'AVC. Dans un modèle d'AVC ischémique chez la souris hyperglycémique, les IO@PDA@tPA ont montré une efficacité similaire à celle du r-tPA sans augmenter le risque hémorragique, une complication courante du r-tPA libre. De plus, une récupération fonctionnelle complète a été observée cinq jours après l'AVC. Ainsi, les IO@PDA@tPA représentent un outil théranostique prometteur pour cibler les microthrombi cérébraux, réduire la dose de r-tPA nécessaire et les effets secondaires associés
There is emerging evidence suggesting that ischemic stroke is frequently associated with the formation of microthrombi in downstream microcirculation. These microthrombi are associated with increased lesion size, cognitive decline, and dementia. Unfortunately, these microthrombi are difficult to detect with current imaging methods. To address this, a novel theranostic agent was developed, IO@PDA@tPA, combining iron oxide microparticles (IO) coated with polydopamine (PDA) and conjugated with recombinant tissue-type plasminogen activator (r-tPA). This agent exhibits in vitro clot lysis activity and reduces reactive oxygen species in neurons under oxygen-glucose deprivation. In vivo, administration of IO@PDA@tPA at one-quarter of the standard r-tPA dose enabled microthrombi visualization and degradation as detected by T2*-weighted magnetic resonance imaging (MRI). This treatment significantly reduced lesion size and promoted recanalization 24 hours after stroke onset. In a hyperglycemic mouse model of IS, the agent showed similar efficacy compared to r-tPA without increasing hemorrhagic risk, a common complication of free r-tPA. Additionally, full functional recovery was observed within five days post-stroke. Thus, IO@PDA@tPA represents a promising theranostic tool for targeting cerebral microthrombi, reducing the required r-tPA dose and associated side effects
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Book chapters on the topic "Microthrombi"

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de Chickera, Sonali N., and Shaifali Sandal. "Kidney Grafts with Evidence of Microthrombi in Glomerular Capillaries." In Complications in Kidney Transplantation, 63–70. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-13569-9_11.

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Shimamura, Kayako, Kuniyuki Oka, Masaki Nakazawa, and Mizu Kojima. "DISTRIBUTION PATTERNS OF MICROTHROMBI IN DISSEMINATED INTRAVASCULAR COAGULATION (DIC)." In Acute pulmonary insufficiency, edited by Tom Saldeen, 103–18. Berlin, Boston: De Gruyter, 1985. http://dx.doi.org/10.1515/9783110850123-007.

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Ghugare, Sheetal Anil, Kusum D. Jashnani, Lalita Yoganand Patil, and Vandana Rajesh Saravade. "Disseminated Microthrombi in Pregnancy: Not Always DIC, Think of TTP." In Maternal Mortality - Lessons Learnt from Autopsy, 87–91. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-3420-9_17.

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Leach, Richard. "The Respiratory System." In Oxford Textbook of Respiratory Critical Care, 7–18. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/med/9780198766438.003.0002.

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Abstract Summary This chapter reviews lung anatomy, including alveolar microanatomy, pulmonary mechanics, control of breathing, gas exchange, pulmonary circulation, and, although not directly related to the respiratory system, the transport of oxygen to the tissues. It examines lung ventilation–perfusion and heart–lung interactions, the impact of low atmospheric pressure and respiratory disease on these relationships. Finally, it briefly acknowledges the many other respiratory system functions, including chemical and drug clearance from the systemic circulation, breakdown of microthrombi, hormone activation (e.g. conversion of angiotensin I to angiotensin II), speech generation, and immune protection. The chapter is divided into the following sections: Introduction, Gross Anatomy of the Lungs and Respiratory Tract, Pulmonary Mechanics, Alveolar Microstructure and Micromechanics, Gas Exchange and Control of Breathing, Pulmonary Circulation, Oxygen Delivery, Heart–Lung Interactions, and Other Lung Functions.
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Prasad, Kuruswamy Thurai. "COVID-19 and Pulmonary Diseases." In COVID-19: Effects in Comorbidities and Special Populations, 230–62. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815036367122010010.

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The coronavirus disease 2019 (COVID-19) primarily affects the respiratory system, commonly manifesting as pneumonia. The clinical presentation of COVID-19 is challenging to distinguish from community-acquired pneumonia due to other etiologies and respiratory exacerbations of pre-existing chronic respiratory diseases. Fortunately, the majority of patients have an asymptomatic or mild illness. However, some patients may develop profound hypoxemia secondary to diffuse alveolar damage and occlusion of alveolar capillaries by microthrombi. When patients with compromised lung function due to pre-existing respiratory diseases develop this disease, they face a setback. The management of the pre-existing illness is often suboptimal due to COVID-19-related restrictions. Further, these patients are more likely to develop severe manifestations of COVID-19 resulting in more severe morbidity and mortality. Diagnosis is established by performing a reverse transcription-polymerase chain reaction (RT-PCR) on samples from the respiratory tract. Treatment of the mild disease is primarily supportive, while supplemental oxygen and mechanical ventilation may be indicated for more severe cases. Several treatment options, including antiviral agents, corticosteroids, immunomodulators, and convalescent plasma therapy, are being investigated. Currently, there is no evidence to indicate that the diagnosis and treatment of COVID-19 are different in those with preexisting respiratory conditions. In the absence of an effective antiviral agent or vaccine, disease prevention is assumed to be of paramount importance. Social distancing and proper use of personal protective equipment are critical in the prevention of transmission.
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Conference papers on the topic "Microthrombi"

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Santos, João Vitor Ribeiro dos, Mariana Spitz, and Ana Carolina Andorinho. "Stroke secondary to thrombotic microangiopathy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.300.

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Introduction: Thrombotic thrombocytopenic purpura (TTP) is a hematological disease resulting from the ADAMTS 13 plasmatic protein deficit. It can be congenital or sporadic, and is usually autoimmune. Pathological platelet adhesion occurs, leading to microthrombi in capillary and arterial circulation, microangiopathic anemia and ischemia. The clinical picture includes thrombocytopenia, renal dysfunction, fluctuating neurological symptoms, microangiopathic hemolytic anemia, and fever. Methods: Case report of a 51-year-old male hypertensive patient, diagnosed with idiopathic thrombocytopenic purpura (ITP) 10 years ago and submitted to splenectomy 5 years ago, who developed acute cholecystitis. He underwent urgent colecistectomy, and on the fourth postoperative day presented sudden space and time disorientation, transcortical motor aphasia and right faciobrachial paresis, with ipsilateral Babinski and Hoffman signs. Results: Brain CT showed left frontoparietal hypodensity. During hospitalization, there was worsening of renal function, increased LDH, and thrombocytopenia. Hematoscopy identified signs of intravascular hemolysis (erythrocyte fragmentation, reticulocytosis, helmet erythrocytes). Direct Coombs was negative. There was no history of heparin use. TTP was diagnosed, and fresh frozen plasma and prednisone 1mg/kg were prescribed. There was resolution of thrombotic microangiopathy, with subsequent increase of platelet levels, decreased LDH and improved hematoscopy. Conclusions: This case illustrates a rare cause of stroke and an unusual association of two hematological conditions: ITP and TTP. The treatment of TTP consists of replacement of deficient ADAMTS13 protein through plasmapheresis or fresh frozen plasma. The use of immunosuppressants is also associated, initially with glucocorticoids, followed by rituximab or splenectomy in order to prevent recurrences.
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Kanamori, Y., I. Yada, I. Yuasa, M. Kusagawa, and K. Deguchi. "PHYSIOLOGICAL ROLE OF THE ENHANCED FIBRINOLYTIC ACTIVITY DURING CARDIOPULMONARY BYPASS IN OPEN HEART SURGERY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644658.

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Fibrinolytic activity is reportedly increased during cardiopulmonary bypass( CPB ), and this increase has been considered to be related to the bleeding complications in open heart surgery. The purpose of this study was to clarify the nature of the fibrinolytic activity duringCPB. Twenty patients with valve replacement or aortocoronary bypass surgery were examined. The following parameters were determined: fibrinogen, plasminogen, fibrinopeptide A( FPA ), fibrinopeptide B β 15-42 ( FPB β15-42 ), and tissue-type plasminogen activator ( t-PA ). For further characterization of the fibrinolytic activity, the fibrin plate method was used. Intrinsic fibrinolytic activity was determined by the assay of the fibrinolytic activity of the kaolin activatedeuglobulin. Extrinsic fibrinolyticactivity was estimated by the assayof Cl-inactivator resistant fibrinolytic activity as well as t-PA. Fibrinogen and plasminogen did not decrease except at the beginning of CPB. FPA was increased significantly during CPB. FPB3 15-42 was also increased to four times the preoperative value at 2 hrs of CPB. The intrinsic fibrinolytic system was activatedonly a short time after the startof CPB. The Cl-inactivator resistant fibrinolytic activity was activated gradually during CPB, reached a maximum level 1 hr after the start of CPB, and returned to the preoperative level within 1 hr after the end of CPB. The changes on t-PA paralleled the course of the Cl-inactivator resistant fibrinolytic activity, indicating that enhanced fibrinolytic activity during CPB is predominantly of extrinsic origin caused by t-PA. We conclude that thrombin activity continues during CPB despite the use of heparin, and thatthe enhanced fibrinolytic activity during CPB is essential because t-PA activates plasminogen predominantly at the sites where fibrin is formed, resulting in the dissolution of the microthrombi formed during CPB.
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Perktold, Karl, Gerhard Karner, and Gerhard Rappitsch. "Flow Effects on the Concentration of Platelet Active Substances in the Vicinity of Mural Platelet Aggregates." In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1228.

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Abstract The influence of convective flow on the transport of prothrombin, thrombin, antithrombin, ADP and thromboxane in the vicinity of a mural microthrombus has been analysed applying computer simulation. The basis of the study is a suitable reaction, emission and transport model. The reaction kinetics and the mass transport are modelled mathematically with a coupled system of convection-diffusion equations. The description of the flow field near the microthrombus uses the three-dimensional Navier-Stokes equations. The numerical approach applies the finite element method.
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Conhaim, RL, KE Watson, WF Dovi, and BA Harms. "Microthrombus Formation Continues in Rat Lungs for up to 24 Hours Following Acute Hemorrhage." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3870.

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Araújo, Victor Oliveira, Isadora Mônica Ponte de Oliveira, Lara Maria de Oliveira Paiva Freitas, and Júlio César Claudino dos Santos. "“Brain fog” in the post-acute phase of Covid-19." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.681.

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Introduction: Covid-19 infection can affect not only the airways but also other organs such as the brain. Individuals that tested positive for SARSCoV-2 may be asymptomatic, but can also have symptoms - such as “brain fog” - during the acute phase and/or the post-acute phase (being the last ones defined as long haulers). “Brain fog” is a set of symptoms characterized by cognitive dysfunction that includes the inability to concentrate, executive function deficits, anterograde and retrograde amnesia. Objective: Review the pathophysiology of individuals with Covid-19 post-acute phase brain fog. Design and setting: A literature review was conducted on the topic. Methods: 12 original selected articles in English and Portuguese from PubMed and Google Academic databases dated from 2017 to 2021. Results: Research evidenced that 18-36% of the patients hospitalized for Covid-19 that had neurological symptoms also experienced brain fog in the post-acute phase. Although not completely elucidated, there are hypothesized mechanisms to clarify the neurological symptoms in the “long haulers’’ patients, such as the release of pro-inflammatory substances that reduce synaptic fidelity due to dysregulation in the levels of neurotransmitters which are fundamental for brain function. In addition, SARS-CoV-2 provides microthrombus formation and possible small cerebral ischemia. Conclusion: The pathophysiology of brain fog is not yet fully proven, since the literature on the subject is limited. Therefore, more robust research in patients who developed neurological symptoms after infection by the new coronavirus is needed to clarify the pathophysiology, clinical management and most appropriate treatment for individuals with brain fog.
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Fujimori, T., T. Saeki, K. Harada, M. Sato, and N. Ohshima. "ANTI-THROMBOTIC EFFECTS OF E-5510 IN EXPERIMENTAL THROMBOSIS MODELS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643429.

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A new agent developed in our laboratory, 4-cyano-5,5-bis(4-methoxyphenyl)-4-pentenoic acid (E-5510), suppressed various human platelet functions in vitro. The compound also showed quite potent ex vivo anti-platelet effects in many experimentalanimals. It is well known that anti-platelet effects are not always parallel to anti-thrombotic effects. Thus, in order to predict the efficacy of E-5510 in thrombotic disorders, the anti-thrombotic effects were examined in 3 different animal models of thrombosis.(1) Anti-thrombotic effect in an extracorporeal shunt model Two hrs after oral administration of the drug to guinea pigs,an extracorporeal shunt between the right carotid artery and the left jugular vein was performed. The thrombus formation on a silk thread inserted in the shunt tube was quantitated by measuring the time from the onset of circulation to the stenosis of blood flow. E-5510 dose-dependently inhibited thrombus formation, the minimum effective dose being 0.03 mg/kg.(2) Effect on microthrombus formation in mesenteric arteriole In order to evaluate the effect on intravascular platelet thrombus formation, thrombosis was induced in vivo in mesenteric arteriole in guinea pigs with filtered light from a mercury lamp and an intravenous fluorescent dye in an intravital microscope system (M. Sato and N. Ohshima, Thromb. Res.,35, 319, 1984). The thrombus formation was quantitated by measuring the time taken for circulating platelets to begin to adhere to vessel wall and the time taken for blood flow to stop completely due to fully developed thrombus. Both the time required for platelet adhesion to vessel wall and for platelet thrombus formation were significantly prolonged after oral administration of E-5510.(3) Effect on pulmonary thromboembolism Acute pulmonary thromboembolism was induced in mice by a bolus intravenous injection of arachidonic acid, and mortality was determined 3 min later. E-5510 dose-dependently reduced pulmonary thromboembolic mortality, and its ED50 was 0.11 mg/kg. The results described above indicate thatE-5510 may have beneficial effects in clinical treatments of thrombotic disease.
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