During acute exercise both coagulant and fibrinolytic potential increase. Since strenuous exertion is associated with an enhanced risk for cardiac events, especially in untrained individuals, it is important to determine whether the initial haemostatic balance is maintained during exercise. Twenty-nine sedentary males (20-30 years) were subjected to a standardized cycle ergometer test. Blood samples were obtained at two exercise levels, 70% VO2max (submaximal), 100% VO2max (maximal) and during 25 min recovery. Both during submaximal and maximal performance, tissue type plasminogen activator antigen, urokinase plasminogen activator antigen and tissue type plasminogen activator activity were increased. A concomitant enhancement of clotting activity of factors VII, VIII, IX, XII and fibrinogen resulted in a shortening of clotting times. Following correction for changes in plasma volume, the results for factor VII:c were reversed, and factor XII:c and fibrinogen no longer demonstrated exercise-related changes. Increases in coagulant (activated partial thromboplastin time) and fibrinolytic (tissue type plasminogen activator activity) potential proceeded in parallel during exercise. However, during recovery while there was a sustained increase in coagulant potential, fibrinolytic potential demonstrated a sharp fall. We conclude that during physical activity, while parallel changes in coagulant and fibrinolytic activity occur, this haemostatic balance is not maintained during recovery. This phenomenon could constitute an enhanced risk for coronary artery thrombosis which may contribute to exercise-related cardiovascular events.
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http://dx.doi.org/10.1093/oxfordjournals.eurheartj.a060859 | DOI Listing |
Cureus
December 2024
Internal Medicine Department, Hospital Beatriz Ângelo, ULS Loures Odivelas, Loures, PRT.
Plasminogen activator inhibitor-1 (PAI-1) is central to fibrinolysis regulation, and genetic variants such as the 4G/4G genotype predispose individuals to hypercoagulability. This case highlights a 46-year-old female patient presenting with acute mesenteric venous thrombosis, where genetic evaluation revealed homozygosity for the PAI-1 4G/4G polymorphism. Management with unfractionated heparin followed by a transition to direct oral anticoagulants led to clinical resolution.
View Article and Find Full Text PDFJuntendo Iji Zasshi
December 2024
Trauma-induced coagulopathy (TIC) is characterized by dynamic changes in fibrinolysis, which can significantly impact patient outcomes. These changes typically manifest in two phases: hyperfibrinolysis followed by fibrinolysis suppression. In the early stages of TIC, there is often an overwhelming release of tissue plasminogen activator, which leads to excessive fibrinolysis.
View Article and Find Full Text PDFFront Neurol
January 2025
Department of Neurology and Institute of Neurology of First Affiliated Hospital, Institute of Neuroscience, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, China.
Introduction: Hemorrhagic transformation (HT) is a severe complication in patients with acute ischemic stroke due to large vessel occlusion (AIS-LVO) after endovascular treatment (EVT). We hypothesize that asymmetry of the internal cerebral veins (ICVs) on baseline CT angiogram (CTA) may serve as an adjunctive predictor of HT.
Methods: We conducted a study on consecutive AIS-LVO patients from November 2020 to April 2022.
Prep Biochem Biotechnol
January 2025
Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.
Chinese hamster ovary (CHO) cells represent the most common host system for the expression of high-quality recombinant proteins. The development of stable CHO cell lines used in industrial recombinant protein production often relies on dihydrofolate reductase (DHFR) and glutamine synthetase (GS) amplification systems. Conventional approaches to develop stable cell lines lead to heterogeneous cell populations.
View Article and Find Full Text PDFMol Ther
January 2025
Immune Health, Hunter Medical Research Institute and The University of Newcastle, Newcastle, New South Wales, Australia; Centre for Inflammation, Centenary Institute and University of Technology Sydney, School of Life Sciences, Faculty of Science, Sydney, New South Wales, Australia. Electronic address:
Vitronectin (VTN) is an important extracellular matrix protein in tissue remodeling, but its role in COPD is unknown. We show that VTN regulates tissue remodeling through urokinase plasminogen activator (uPA) signaling pathway in COPD. In human COPD airways and bronchoepithelial cells and the airways of mice with cigarette smoke (CS)-induced experimental COPD, VTN protein was not changed, but downstream uPA signaling was altered (increased plasminogen activator inhibitor-1, uPAR) that induced collagen and airway remodeling.
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