Background: Balloon angioplasty has recently been adopted as an acceptable form of treatment for stenotic vessel lesions of congenital heart diseases. However, precise mechanisms of restenosis and thrombosis, which are the most common complications after these procedures, are unknown.
Methods: We examined the effects of antithrombin III (ATIII) on inflammation, thrombus formation, and remodeling of vascular wall after guidewire-induced injury in the femoral artery of mice. ATIII or saline was administered as a bolus intravenous infusion before injury.
Results: Seventy-two hours after injury, approximately half of the saline-treated vessels showed macroscopic thrombus formation. In contrast, no thrombi were seen in the arteries pretreated with ATIII. Significantly higher levels of inflammation were induced in the injured vessels than in the sham-operated controls, as determined by CD11b-positive cell density in the adventitial area. ATIII treatment resulted in marked reduction of inflammatory cell infiltration. Twenty-eight days after injury, similar levels of neointimal proliferation were found in the injured arteries in both groups.
Conclusions: Our results suggested that a high dose of ATIII may influence the sequelae of arterial injury by reducing mural thrombus formation and limiting the inflammatory reaction of the vessel wall without altering the process of vascular remodeling.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/j.1442-200X.2011.03350.x | DOI Listing |
Physiol Rep
January 2025
Gravitational Physiology and Medicine Research Unit, Division of Physiology, Otto Loewi Research Center, Medical University of Graz, Graz, Austria.
Available evidence suggests that various medical/rehabilitation treatments evoke multiple effects on blood hemostasis. It was therefore the aim of our study to examine whether fascial manipulation, vibration exercise, motor imagery, or neuro-muscular electrical stimulation can activate the coagulation system, and, thereby, expose patients to thrombotic risk. Ten healthy young subject were enrolled in the study.
View Article and Find Full Text PDFZhongguo Shi Yan Xue Ye Xue Za Zhi
December 2024
Jiangsu Institute of Hematology, National Clinical Research Center for Hematologic Diseases, NHC Key Laboratory of Thrombosis and Hemostasis, The First Affiliated Hospital of Soochow University, Collaborative Innovation Center of Hematology, Suzhou 215006, Jiangsu Province, China.
Objective: To study the molecular mechanism of functional defect of protein C (PC) caused by point mutations of human protein C gene ( ) N355S , G392E and T314A.
Methods: The wild-type and mutant plasmids (PC, PC, PC, PC) of gene were constructed and transiently transfected into HEK293 cells. The expression of mutant proteins in vitro were tested.
Front Vet Sci
December 2024
Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, United States.
Introduction: Cardiogenic arterial thromboembolism (CATE) is a life-threatening complication of hypertrophic cardiomyopathy (HCM) with a high mortality rate. As the primary responders in hemostasis, platelets play a crucial role in the progression of CATE. Procoagulant platelets are a subpopulation of activated platelets that facilitate thrombin generation to strengthen thrombus structure.
View Article and Find Full Text PDFMediators Inflamm
January 2025
Program in Translational Medicine, National Chung Hsing University, Taichung, Taiwan.
Antiphospholipid antibody syndrome (APS) is an autoimmune disease characterized by the presence of 2-glycoprotein I (2-GPI)-targeting antiphospholipid antibodies (aPLs) and vascular thrombosis or obstetrical complications. One of its severe manifestations is nephropathy. To examine the role of type I interferon (IFN) and therapeutic potential of tyrosine kinase 2 (Tyk2) inhibition, we administered BMS-986202, a novel Tyk2 inhibitor, in a mouse model of APS nephropathy.
View Article and Find Full Text PDFCardiovasc Ther
January 2025
Department of Biomedical Sciences, Joan C. Edwards School of Medicine at Marshall University, Huntington, West Virginia, USA.
Thymidine phosphorylase (TYMP) promotes platelet activation and thrombosis while suppressing vascular smooth muscle cell (VSMC) proliferation. Both processes are central to the development and progression of abdominal aortic aneurysms (AAAs). We hypothesize that TYMP plays a role in AAA development.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!