Injury Length and Arteriole Constriction Shape Clot Growth and Blood-Flow Acceleration in a Mouse Model of Thrombosis

OBJECTIVE:Quantitative relationships between the extent of injury and thrombus formation in vivo are not well understood. Moreover, it has not been investigated how increased injury severity translates to blood-flow modulation. Here, we investigated interconnections between injury length, clot growt...

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Veröffentlicht in:Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2020-09, Vol.40 (9), p.2114-2126
Hauptverfasser: Mitrophanov, Alexander Y., Merrill-Skoloff, Glenn, Grover, Steven P., Govindarajan, Vijay, Kolanjiyil, Arun, Hariprasad, Daniel S., Unnikrishnan, Ginu, Flaumenhaft, Robert, Reifman, Jaques
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container_end_page 2126
container_issue 9
container_start_page 2114
container_title Arteriosclerosis, thrombosis, and vascular biology
container_volume 40
creator Mitrophanov, Alexander Y.
Merrill-Skoloff, Glenn
Grover, Steven P.
Govindarajan, Vijay
Kolanjiyil, Arun
Hariprasad, Daniel S.
Unnikrishnan, Ginu
Flaumenhaft, Robert
Reifman, Jaques
description OBJECTIVE:Quantitative relationships between the extent of injury and thrombus formation in vivo are not well understood. Moreover, it has not been investigated how increased injury severity translates to blood-flow modulation. Here, we investigated interconnections between injury length, clot growth, and blood flow in a mouse model of laser-induced thrombosis. APPROACH AND RESULTS:Using intravital microscopy, we analyzed 59 clotting events collected from the cremaster arteriole of 14 adult mice. We regarded injury length as a measure of injury severity. The injury caused transient constriction upstream and downstream of the injury site resulting in a 50% reduction in arteriole diameter. The amount of platelet accumulation and fibrin formation did not depend on arteriole diameter or deformation but displayed an exponentially increasing dependence on injury length. The height of the platelet clot depended linearly on injury length and the arteriole diameter. Upstream arteriolar constriction correlated with delayed upstream velocity increase, which, in turn, determined downstream velocity. Before clot formation, flow velocity positively correlated with the arteriole diameter. After the onset of thrombus growth, flow velocity at the injury site negatively correlated with the arteriole diameter and with the size of the above-clot lumen. CONCLUSIONS:Injury severity increased platelet accumulation and fibrin formation in a persistently steep fashion and, together with arteriole diameter, defined clot height. Arterial constriction and clot formation were characterized by a dynamic change in the blood flow, associated with increased flow velocity.
doi_str_mv 10.1161/ATVBAHA.120.314786
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Moreover, it has not been investigated how increased injury severity translates to blood-flow modulation. Here, we investigated interconnections between injury length, clot growth, and blood flow in a mouse model of laser-induced thrombosis. APPROACH AND RESULTS:Using intravital microscopy, we analyzed 59 clotting events collected from the cremaster arteriole of 14 adult mice. We regarded injury length as a measure of injury severity. The injury caused transient constriction upstream and downstream of the injury site resulting in a 50% reduction in arteriole diameter. The amount of platelet accumulation and fibrin formation did not depend on arteriole diameter or deformation but displayed an exponentially increasing dependence on injury length. The height of the platelet clot depended linearly on injury length and the arteriole diameter. Upstream arteriolar constriction correlated with delayed upstream velocity increase, which, in turn, determined downstream velocity. Before clot formation, flow velocity positively correlated with the arteriole diameter. After the onset of thrombus growth, flow velocity at the injury site negatively correlated with the arteriole diameter and with the size of the above-clot lumen. CONCLUSIONS:Injury severity increased platelet accumulation and fibrin formation in a persistently steep fashion and, together with arteriole diameter, defined clot height. Arterial constriction and clot formation were characterized by a dynamic change in the blood flow, associated with increased flow velocity.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/ATVBAHA.120.314786</identifier><language>eng</language><publisher>American Heart Association, Inc</publisher><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2020-09, Vol.40 (9), p.2114-2126</ispartof><rights>American Heart Association, Inc.</rights><rights>2020 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4166-34ca5dafbecaeba87d6390180970a4f4ee79843183f9a45aec1ee45988187acf3</citedby><cites>FETCH-LOGICAL-c4166-34ca5dafbecaeba87d6390180970a4f4ee79843183f9a45aec1ee45988187acf3</cites><orcidid>0000-0002-9019-4034 ; 0000-0001-7292-2029</orcidid></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></links><search><creatorcontrib>Mitrophanov, Alexander Y.</creatorcontrib><creatorcontrib>Merrill-Skoloff, Glenn</creatorcontrib><creatorcontrib>Grover, Steven P.</creatorcontrib><creatorcontrib>Govindarajan, Vijay</creatorcontrib><creatorcontrib>Kolanjiyil, Arun</creatorcontrib><creatorcontrib>Hariprasad, Daniel S.</creatorcontrib><creatorcontrib>Unnikrishnan, Ginu</creatorcontrib><creatorcontrib>Flaumenhaft, Robert</creatorcontrib><creatorcontrib>Reifman, Jaques</creatorcontrib><title>Injury Length and Arteriole Constriction Shape Clot Growth and Blood-Flow Acceleration in a Mouse Model of Thrombosis</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><description>OBJECTIVE:Quantitative relationships between the extent of injury and thrombus formation in vivo are not well understood. Moreover, it has not been investigated how increased injury severity translates to blood-flow modulation. Here, we investigated interconnections between injury length, clot growth, and blood flow in a mouse model of laser-induced thrombosis. APPROACH AND RESULTS:Using intravital microscopy, we analyzed 59 clotting events collected from the cremaster arteriole of 14 adult mice. We regarded injury length as a measure of injury severity. The injury caused transient constriction upstream and downstream of the injury site resulting in a 50% reduction in arteriole diameter. The amount of platelet accumulation and fibrin formation did not depend on arteriole diameter or deformation but displayed an exponentially increasing dependence on injury length. The height of the platelet clot depended linearly on injury length and the arteriole diameter. Upstream arteriolar constriction correlated with delayed upstream velocity increase, which, in turn, determined downstream velocity. Before clot formation, flow velocity positively correlated with the arteriole diameter. After the onset of thrombus growth, flow velocity at the injury site negatively correlated with the arteriole diameter and with the size of the above-clot lumen. CONCLUSIONS:Injury severity increased platelet accumulation and fibrin formation in a persistently steep fashion and, together with arteriole diameter, defined clot height. 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Moreover, it has not been investigated how increased injury severity translates to blood-flow modulation. Here, we investigated interconnections between injury length, clot growth, and blood flow in a mouse model of laser-induced thrombosis. APPROACH AND RESULTS:Using intravital microscopy, we analyzed 59 clotting events collected from the cremaster arteriole of 14 adult mice. We regarded injury length as a measure of injury severity. The injury caused transient constriction upstream and downstream of the injury site resulting in a 50% reduction in arteriole diameter. The amount of platelet accumulation and fibrin formation did not depend on arteriole diameter or deformation but displayed an exponentially increasing dependence on injury length. The height of the platelet clot depended linearly on injury length and the arteriole diameter. Upstream arteriolar constriction correlated with delayed upstream velocity increase, which, in turn, determined downstream velocity. Before clot formation, flow velocity positively correlated with the arteriole diameter. After the onset of thrombus growth, flow velocity at the injury site negatively correlated with the arteriole diameter and with the size of the above-clot lumen. CONCLUSIONS:Injury severity increased platelet accumulation and fibrin formation in a persistently steep fashion and, together with arteriole diameter, defined clot height. Arterial constriction and clot formation were characterized by a dynamic change in the blood flow, associated with increased flow velocity.</abstract><pub>American Heart Association, Inc</pub><doi>10.1161/ATVBAHA.120.314786</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-9019-4034</orcidid><orcidid>https://orcid.org/0000-0001-7292-2029</orcidid><oa>free_for_read</oa></addata></record>
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title Injury Length and Arteriole Constriction Shape Clot Growth and Blood-Flow Acceleration in a Mouse Model of Thrombosis
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