Amanda Sampaio Storch1, Helena Naly Miguens Rocha2, Vinicius Pacheco Garcia3, Gabriel Matheus da Silva Batista4, João Dario Mattos5, Monique Opuszcka Campos6, André Lopes Fuly7, Antonio Claudio Lucas da Nóbrega8, Igor Alexandre Fernandes9, Natália Galito Rocha10. 1. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. Electronic address: asstorch@id.uff.br. 2. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. Electronic address: hmiguens@id.uff.br. 3. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. Electronic address: viniciuspg@id.uff.br. 4. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. Electronic address: gabrielbatista@id.uff.br. 5. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. Electronic address: joaodario@id.uff.br. 6. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. 7. Department of Cellular and Molecular Biology (GCM), Institute of Biology, Fluminense Federal University, Outeiro de São João Batista, s/n, Centro, Niteroi, Rio de Janeiro, Brazil. Electronic address: andrefuly@id.uff.br. 8. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil; National Institute of Science and Technology (INCT) - Physical (In)activity and Exercise, National Council for Scientific and Technological Development (CNPq), Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. Electronic address: anobrega@id.uff.br. 9. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. Electronic address: fernandes.igor@unb.br. 10. Laboratory of Exercise Sciences (LACE), Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil; National Institute of Science and Technology (INCT) - Physical (In)activity and Exercise, National Council for Scientific and Technological Development (CNPq), Fluminense Federal University, Rua Professor Hernani Pires de Melo, 101, Sala 106, São Domingos, Niterói, Rio de Janeiro, Brazil. Electronic address: nataliagalito@id.uff.br.
Abstract
INTRODUCTION: In vitro and animal model studies have demonstrated that oscillatory shear can trigger vascular hemostasis and remodeling. However, the roles of hemodynamic forces in vascular human biology are not well understood. This study aimed to determine the effects of increasing oscillatory shear stress (OSS) on coagulation/fibrinolysis factors and matrix metalloproteinase-9 activity in healthy subjects. MATERIALS AND METHODS: Ten healthy males (35 ± 7 years) underwent a 30-minute dominant forearm cuff occlusion (75 mm Hg) to exacerbate OSS in the brachial artery. Blood flow was quantified (Doppler ultrasound), and plasma samples were obtained from both arms at rest and during the last 30 s of cuff occlusion on the dominant arm. A proximal cuff (40 mm Hg, close to axilla) was also occluded to facilitate venous blood biomarker trapping. RESULTS: The retrograde shear rate and oscillatory shear index were increased and the mean shear rate, mean blood velocity, and mean blood flow were decreased in the cuffed arm (p < 0.05 vs. baseline and non-cuffed arm). Cuff occlusion induced increases in platelet microparticle release (p = 0.05 vs. baseline), prothrombin time (p < 0.05 vs. baseline and non-cuffed arm), tissue plasminogen activator (p < 0.01 vs. baseline and non-cuffed arm), plasminogen activator inhibitor-1 (p < 0.02 vs. baseline and non-cuffed arm), and matrix metalloproteinase-9 activity (p = 0.01 vs. baseline). No significant changes were found in the non-cuffed arm throughout the protocol. CONCLUSIONS: Exacerbation of OSS induced in vivo disturbances in platelet microparticle release, coagulation-fibrinolysis, and matrix metalloproteinase-9 activity in healthy individuals. These are potential mechanisms involved in OSS-mediated endothelial dysfunction.
INTRODUCTION: In vitro and animal model studies have demonstrated that oscillatory shear can trigger vascular hemostasis and remodeling. However, the roles of hemodynamic forces in vascular human biology are not well understood. This study aimed to determine the effects of increasing oscillatory shear stress (OSS) on coagulation/fibrinolysis factors and matrix metalloproteinase-9 activity in healthy subjects. MATERIALS AND METHODS: Ten healthy males (35 ± 7 years) underwent a 30-minute dominant forearm cuff occlusion (75 mm Hg) to exacerbate OSS in the brachial artery. Blood flow was quantified (Doppler ultrasound), and plasma samples were obtained from both arms at rest and during the last 30 s of cuff occlusion on the dominant arm. A proximal cuff (40 mm Hg, close to axilla) was also occluded to facilitate venous blood biomarker trapping. RESULTS: The retrograde shear rate and oscillatory shear index were increased and the mean shear rate, mean blood velocity, and mean blood flow were decreased in the cuffed arm (p < 0.05 vs. baseline and non-cuffed arm). Cuff occlusion induced increases in platelet microparticle release (p = 0.05 vs. baseline), prothrombin time (p < 0.05 vs. baseline and non-cuffed arm), tissue plasminogen activator (p < 0.01 vs. baseline and non-cuffed arm), plasminogen activator inhibitor-1 (p < 0.02 vs. baseline and non-cuffed arm), and matrix metalloproteinase-9 activity (p = 0.01 vs. baseline). No significant changes were found in the non-cuffed arm throughout the protocol. CONCLUSIONS: Exacerbation of OSS induced in vivo disturbances in platelet microparticle release, coagulation-fibrinolysis, and matrix metalloproteinase-9 activity in healthy individuals. These are potential mechanisms involved in OSS-mediated endothelial dysfunction.
Authors: V P Garcia; J D Mattos; J Mentzinger; P E C Leite; H N M Rocha; M O Campos; M P Rocha; D E Mansur; N H Secher; A C L Nóbrega; I A Fernandes; N G Rocha Journal: Braz J Med Biol Res Date: 2022-06-13 Impact factor: 2.904
Authors: Amanda S Storch; Helena N M Rocha; Vinicius P Garcia; Gabriel M S Batista; João Dario Mattos; Monique O Campos; Antonio Claudio L Nóbrega; Igor A Fernandes; Natalia G Rocha Journal: Hypertens Res Date: 2019-06-28 Impact factor: 3.872