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Orthostatic Hypercoagulability: A Novel Physiological Mechanism to Activate the Coagulation System
Orthostatic stress causes significant plasma shift and raises transmural pressure in lower extremities, resulting in an increase in endothelial activation and plasma proteins concentrations, possibly including coagulation factors. This may lead to activation of the coagulation system during standing...
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| Published in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2008-06, Vol.51 (6), p.1545-1551 |
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| Language: | English |
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| container_end_page | 1551 |
| container_issue | 6 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Masoud, Muhannad Sarig, Galit Brenner, Benjamin Jacob, Giris |
| description | Orthostatic stress causes significant plasma shift and raises transmural pressure in lower extremities, resulting in an increase in endothelial activation and plasma proteins concentrations, possibly including coagulation factors. This may lead to activation of the coagulation system during standing. To test this hypothesis, we recruited 18 healthy volunteers (9 females and 9 males; mean age25±1.2 years; body mass index21.7±0.5 kg/m). Hemodynamics, plasma shift (extrapolated from sequential hematocrit concentration), plasma proteins, and coagulation tests, including procoagulants; fibrinogen, factor V, and factor VIII activity; prothrombin fragments 1 and 2; and endothelial activation–related factors (tissue factor and von Willebrand factor), as well as protein C global pathway, were determined at rest supine and at 15 minutes, 30 minutes, and 60 minutes of still standing. Thirty minutes of standing caused a decrease in plasma volume by 12.0±0.5% and an increase in plasma protein by 13.0±0.7%. Fibrinogen, factor V, and factor VIII activity rose by 12.0±1.2%, 13.0±1.0%, and 40.0±6.0% (P |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.108.112003 |
| format | article |
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This may lead to activation of the coagulation system during standing. To test this hypothesis, we recruited 18 healthy volunteers (9 females and 9 males; mean age25±1.2 years; body mass index21.7±0.5 kg/m). Hemodynamics, plasma shift (extrapolated from sequential hematocrit concentration), plasma proteins, and coagulation tests, including procoagulants; fibrinogen, factor V, and factor VIII activity; prothrombin fragments 1 and 2; and endothelial activation–related factors (tissue factor and von Willebrand factor), as well as protein C global pathway, were determined at rest supine and at 15 minutes, 30 minutes, and 60 minutes of still standing. Thirty minutes of standing caused a decrease in plasma volume by 12.0±0.5% and an increase in plasma protein by 13.0±0.7%. Fibrinogen, factor V, and factor VIII activity rose by 12.0±1.2%, 13.0±1.0%, and 40.0±6.0% (P<0.002 for all), respectively. Prothrombin fragments 1 and 2 were elevated by 150.0±30.0%. Tissue factor and von Willebrand factor increased by 30.0±9.0% and 17.4±51.0% (P<0.02 for both), respectively. However, protein C assay results decreased from 0.95±0.20 to 0.83±0.16 (P<0.001). We hereby introduce a novel physiological mechanism, “orthostatic procoagulation,” that should be considered during coagulation tests. Furthermore, it could be extrapolated to the pathophysiology of stasis and venous thromboembolism.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.108.112003</identifier><identifier>PMID: 18413485</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Adult ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Coagulation - physiology ; Blood Pressure - physiology ; Cardiology. Vascular system ; Endocrine kidney. Renin-angiotensin-aldosterone system ; Endothelium, Vascular - physiology ; Factor V - metabolism ; Factor VIII - metabolism ; Female ; Fibrinogen - metabolism ; Fundamental and applied biological sciences. Psychology ; Hematocrit ; Humans ; Male ; Medical sciences ; Peptide Fragments - metabolism ; Plasma Volume - physiology ; Posture ; Protein C - metabolism ; Protein Precursors - metabolism ; Prothrombin - metabolism ; Thrombophilia - physiopathology ; Thromboplastin - metabolism ; Venous Thromboembolism - physiopathology ; Vertebrates: endocrinology ; von Willebrand Factor - metabolism</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2008-06, Vol.51 (6), p.1545-1551</ispartof><rights>2008 American Heart Association, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3774-915675808745b50e65c0c69b497fbc35fe79e3936848c1a8e00149470abc3f233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20393117$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18413485$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Masoud, Muhannad</creatorcontrib><creatorcontrib>Sarig, Galit</creatorcontrib><creatorcontrib>Brenner, Benjamin</creatorcontrib><creatorcontrib>Jacob, Giris</creatorcontrib><title>Orthostatic Hypercoagulability: A Novel Physiological Mechanism to Activate the Coagulation System</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Orthostatic stress causes significant plasma shift and raises transmural pressure in lower extremities, resulting in an increase in endothelial activation and plasma proteins concentrations, possibly including coagulation factors. This may lead to activation of the coagulation system during standing. To test this hypothesis, we recruited 18 healthy volunteers (9 females and 9 males; mean age25±1.2 years; body mass index21.7±0.5 kg/m). Hemodynamics, plasma shift (extrapolated from sequential hematocrit concentration), plasma proteins, and coagulation tests, including procoagulants; fibrinogen, factor V, and factor VIII activity; prothrombin fragments 1 and 2; and endothelial activation–related factors (tissue factor and von Willebrand factor), as well as protein C global pathway, were determined at rest supine and at 15 minutes, 30 minutes, and 60 minutes of still standing. Thirty minutes of standing caused a decrease in plasma volume by 12.0±0.5% and an increase in plasma protein by 13.0±0.7%. Fibrinogen, factor V, and factor VIII activity rose by 12.0±1.2%, 13.0±1.0%, and 40.0±6.0% (P<0.002 for all), respectively. Prothrombin fragments 1 and 2 were elevated by 150.0±30.0%. Tissue factor and von Willebrand factor increased by 30.0±9.0% and 17.4±51.0% (P<0.02 for both), respectively. However, protein C assay results decreased from 0.95±0.20 to 0.83±0.16 (P<0.001). We hereby introduce a novel physiological mechanism, “orthostatic procoagulation,” that should be considered during coagulation tests. Furthermore, it could be extrapolated to the pathophysiology of stasis and venous thromboembolism.</description><subject>Adult</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Coagulation - physiology</subject><subject>Blood Pressure - physiology</subject><subject>Cardiology. Vascular system</subject><subject>Endocrine kidney. Renin-angiotensin-aldosterone system</subject><subject>Endothelium, Vascular - physiology</subject><subject>Factor V - metabolism</subject><subject>Factor VIII - metabolism</subject><subject>Female</subject><subject>Fibrinogen - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hematocrit</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Peptide Fragments - metabolism</subject><subject>Plasma Volume - physiology</subject><subject>Posture</subject><subject>Protein C - metabolism</subject><subject>Protein Precursors - metabolism</subject><subject>Prothrombin - metabolism</subject><subject>Thrombophilia - physiopathology</subject><subject>Thromboplastin - metabolism</subject><subject>Venous Thromboembolism - physiopathology</subject><subject>Vertebrates: endocrinology</subject><subject>von Willebrand Factor - metabolism</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNpdkGFr2zAQhsXYWLOuf2GIwfbNnWTJltxvJmRLoUtK20H3ycjaudYmR6kkt_jfT8FhgwoOobvnvdO9CH2k5JzSkn5Z_7xe3dytNreX2029rs8pkamQE8JeoQUtcp7xomSv0YLQimcVpfcn6F0IvwmhnHPxFp1QySnjsligdutj70JU0Wi8nvbgtVMPo1WtsSZOF7jGG_cEFl_3UzDOugejlcXfQfdqZ8KAo8O1juZJRcCxB7yc5dG4Hb6dQoThPXrTKRvg7Hifoh9fV3fLdXa1_Xa5rK8yzYQ4_LMoRSGJFLxoCwJloYkuq5ZXoms1KzoQFbCKlZJLTZWEwzoVF0Slapczdoo-z3333j2OEGIzmKDBWrUDN4ZGkNS-InkCL2ZQexeCh67ZezMoPzWUNAeHmxcOp7xsZoeT-MNxytgO8Ou_9GhpAj4dARWSVZ1XO23CPy4naQdKReL4zD07G8GHP3Z8Bt_0oGzsG5IOz0uZpaGSlOmVpcg5-wtUeZXO</recordid><startdate>200806</startdate><enddate>200806</enddate><creator>Masoud, Muhannad</creator><creator>Sarig, Galit</creator><creator>Brenner, Benjamin</creator><creator>Jacob, Giris</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200806</creationdate><title>Orthostatic Hypercoagulability: A Novel Physiological Mechanism to Activate the Coagulation System</title><author>Masoud, Muhannad ; Sarig, Galit ; Brenner, Benjamin ; Jacob, Giris</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3774-915675808745b50e65c0c69b497fbc35fe79e3936848c1a8e00149470abc3f233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Coagulation - physiology</topic><topic>Blood Pressure - physiology</topic><topic>Cardiology. Vascular system</topic><topic>Endocrine kidney. Renin-angiotensin-aldosterone system</topic><topic>Endothelium, Vascular - physiology</topic><topic>Factor V - metabolism</topic><topic>Factor VIII - metabolism</topic><topic>Female</topic><topic>Fibrinogen - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hematocrit</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Peptide Fragments - metabolism</topic><topic>Plasma Volume - physiology</topic><topic>Posture</topic><topic>Protein C - metabolism</topic><topic>Protein Precursors - metabolism</topic><topic>Prothrombin - metabolism</topic><topic>Thrombophilia - physiopathology</topic><topic>Thromboplastin - metabolism</topic><topic>Venous Thromboembolism - physiopathology</topic><topic>Vertebrates: endocrinology</topic><topic>von Willebrand Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Masoud, Muhannad</creatorcontrib><creatorcontrib>Sarig, Galit</creatorcontrib><creatorcontrib>Brenner, Benjamin</creatorcontrib><creatorcontrib>Jacob, Giris</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Masoud, Muhannad</au><au>Sarig, Galit</au><au>Brenner, Benjamin</au><au>Jacob, Giris</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Orthostatic Hypercoagulability: A Novel Physiological Mechanism to Activate the Coagulation System</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2008-06</date><risdate>2008</risdate><volume>51</volume><issue>6</issue><spage>1545</spage><epage>1551</epage><pages>1545-1551</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Orthostatic stress causes significant plasma shift and raises transmural pressure in lower extremities, resulting in an increase in endothelial activation and plasma proteins concentrations, possibly including coagulation factors. This may lead to activation of the coagulation system during standing. To test this hypothesis, we recruited 18 healthy volunteers (9 females and 9 males; mean age25±1.2 years; body mass index21.7±0.5 kg/m). Hemodynamics, plasma shift (extrapolated from sequential hematocrit concentration), plasma proteins, and coagulation tests, including procoagulants; fibrinogen, factor V, and factor VIII activity; prothrombin fragments 1 and 2; and endothelial activation–related factors (tissue factor and von Willebrand factor), as well as protein C global pathway, were determined at rest supine and at 15 minutes, 30 minutes, and 60 minutes of still standing. Thirty minutes of standing caused a decrease in plasma volume by 12.0±0.5% and an increase in plasma protein by 13.0±0.7%. Fibrinogen, factor V, and factor VIII activity rose by 12.0±1.2%, 13.0±1.0%, and 40.0±6.0% (P<0.002 for all), respectively. Prothrombin fragments 1 and 2 were elevated by 150.0±30.0%. Tissue factor and von Willebrand factor increased by 30.0±9.0% and 17.4±51.0% (P<0.02 for both), respectively. However, protein C assay results decreased from 0.95±0.20 to 0.83±0.16 (P<0.001). We hereby introduce a novel physiological mechanism, “orthostatic procoagulation,” that should be considered during coagulation tests. Furthermore, it could be extrapolated to the pathophysiology of stasis and venous thromboembolism.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>18413485</pmid><doi>10.1161/HYPERTENSIONAHA.108.112003</doi><tpages>7</tpages></addata></record> |
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| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2008-06, Vol.51 (6), p.1545-1551 |
| issn | 0194-911X 1524-4563 |
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| subjects | Adult Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Coagulation - physiology Blood Pressure - physiology Cardiology. Vascular system Endocrine kidney. Renin-angiotensin-aldosterone system Endothelium, Vascular - physiology Factor V - metabolism Factor VIII - metabolism Female Fibrinogen - metabolism Fundamental and applied biological sciences. Psychology Hematocrit Humans Male Medical sciences Peptide Fragments - metabolism Plasma Volume - physiology Posture Protein C - metabolism Protein Precursors - metabolism Prothrombin - metabolism Thrombophilia - physiopathology Thromboplastin - metabolism Venous Thromboembolism - physiopathology Vertebrates: endocrinology von Willebrand Factor - metabolism |
| title | Orthostatic Hypercoagulability: A Novel Physiological Mechanism to Activate the Coagulation System |
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