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    On the Subclavian Steal Syndrome In Vitro Studies

    Source: Journal of Biomechanical Engineering:;1992:;volume( 114 ):;issue: 004::page 527
    Author:
    C. M. Rodkiewicz
    ,
    S. Zajac
    ,
    J. Centkowski
    DOI: 10.1115/1.2894106
    Publisher: The American Society of Mechanical Engineers (ASME)
    Abstract: An elastic model of the arterial system has been used in which a specially designed pumping unit simulated the heart action. Physiological pressures and normal geometry, size, and flow distribution together with the normal cardiac output and use of prosthetic heart valves are the features of the system. Atherosclerosis was simulated by introducing blockages of known cross-section at specific sites of predilection. It has been shown that, for some specific occlusion magnitude in the left or right subclavian, or in the brachycephalic arteries, the stagnant no blood flow condition will appear in the left vertebral, or the right vertebral, or right common carotid, or the right internal carotid arteries. For larger occlusions the blood flow in these arteries reverses its direction, i.e., the “steal syndrome” appears. It is shown that besides the known single steal syndrome there exists also a double steal syndrome, i.e., blood reverses its flow direction simultaneously in two arteries, both on the right side of the arterial system. This blood is taken from the circle of Willis, which at the same time is significantly supplemented by the increased blood flow through the other arteries leading into the circle of Willis.
    keyword(s): Flow (Dynamics) , Blood , Geometry , Heart valve prostheses , Physiology , Atherosclerosis , Carotid arteries AND Blood flow ,
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      On the Subclavian Steal Syndrome In Vitro Studies

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    http://yetl.yabesh.ir/yetl1/handle/yetl/109821
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    contributor authorC. M. Rodkiewicz
    contributor authorS. Zajac
    contributor authorJ. Centkowski
    date accessioned2017-05-08T23:37:40Z
    date available2017-05-08T23:37:40Z
    date copyrightNovember, 1992
    date issued1992
    identifier issn0148-0731
    identifier otherJBENDY-25891#527_1.pdf
    identifier urihttp://yetl.yabesh.ir/yetl/handle/yetl/109821
    description abstractAn elastic model of the arterial system has been used in which a specially designed pumping unit simulated the heart action. Physiological pressures and normal geometry, size, and flow distribution together with the normal cardiac output and use of prosthetic heart valves are the features of the system. Atherosclerosis was simulated by introducing blockages of known cross-section at specific sites of predilection. It has been shown that, for some specific occlusion magnitude in the left or right subclavian, or in the brachycephalic arteries, the stagnant no blood flow condition will appear in the left vertebral, or the right vertebral, or right common carotid, or the right internal carotid arteries. For larger occlusions the blood flow in these arteries reverses its direction, i.e., the “steal syndrome” appears. It is shown that besides the known single steal syndrome there exists also a double steal syndrome, i.e., blood reverses its flow direction simultaneously in two arteries, both on the right side of the arterial system. This blood is taken from the circle of Willis, which at the same time is significantly supplemented by the increased blood flow through the other arteries leading into the circle of Willis.
    publisherThe American Society of Mechanical Engineers (ASME)
    titleOn the Subclavian Steal Syndrome In Vitro Studies
    typeJournal Paper
    journal volume114
    journal issue4
    journal titleJournal of Biomechanical Engineering
    identifier doi10.1115/1.2894106
    journal fristpage527
    journal lastpage532
    identifier eissn1528-8951
    keywordsFlow (Dynamics)
    keywordsBlood
    keywordsGeometry
    keywordsHeart valve prostheses
    keywordsPhysiology
    keywordsAtherosclerosis
    keywordsCarotid arteries AND Blood flow
    treeJournal of Biomechanical Engineering:;1992:;volume( 114 ):;issue: 004
    contenttypeFulltext
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