{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,25]],"date-time":"2026-07-25T22:07:20Z","timestamp":1785017240730,"version":"3.55.0"},"reference-count":56,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,11,5]],"date-time":"2013-11-05T00:00:00Z","timestamp":1383609600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>A spinal cord injury (<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>) clearly results in greater cardiovascular risk; however, accompanying changes in peripheral vascular structure below the lesion mean that the real impact of a<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>on vascular function is unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aim<\/jats:title><jats:p>Therefore, utilizing passive leg movement\u2010induced (<jats:styled-content style=\"fixed-case\">PLM<\/jats:styled-content>) hyperaemia, an index of nitric oxide (<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>)\u2010dependent vascular function and the central hemodynamic response to this intervention, we studied eight individuals with a<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>and eight age\u2010matched controls (<jats:styled-content style=\"fixed-case\">CTRL<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Specifically, we assessed heart rate (<jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>), stroke volume (<jats:styled-content style=\"fixed-case\">SV<\/jats:styled-content>), cardiac output (<jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>), mean arterial pressure (<jats:styled-content style=\"fixed-case\">MAP<\/jats:styled-content>), leg blood flow (<jats:styled-content style=\"fixed-case\">LBF<\/jats:styled-content>) and thigh composition.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In<jats:styled-content style=\"fixed-case\">CTRL<\/jats:styled-content>, passive movement transiently decreased<jats:styled-content style=\"fixed-case\">MAP<\/jats:styled-content>and increased<jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>from baseline by 2.5\u00a0\u00b1\u00a01\u00a0mmHg, 7\u00a0\u00b1\u00a02\u00a0bpm and 0.5\u00a0\u00b1\u00a00.1\u00a0L\u00a0min<jats:sup>\u22121<\/jats:sup>respectively. In<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>responses were unidentifiable.<jats:styled-content style=\"fixed-case\">LBF<\/jats:styled-content>increased to a greater extent in<jats:styled-content style=\"fixed-case\">CTRL<\/jats:styled-content>(515\u00a0\u00b1\u00a041\u00a0\u2206mL\u00a0min<jats:sup>\u22121<\/jats:sup>) compared with<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>, (126\u00a0\u00b1\u00a025\u00a0\u2206mL\u00a0min<jats:sup>\u22121<\/jats:sup>) (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05). There was a strong relationship between \u2206<jats:styled-content style=\"fixed-case\">LBF<\/jats:styled-content>and thigh muscle volume (<jats:italic>r<\/jats:italic>\u00a0=\u00a00.95). After normalizing \u2206<jats:styled-content style=\"fixed-case\">LBF<\/jats:styled-content>for this strong relationship (\u2206<jats:styled-content style=\"fixed-case\">LBF<\/jats:styled-content>\/muscle volume), there was evidence of preserved vascular function in<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>(<jats:styled-content style=\"fixed-case\">CTRL<\/jats:styled-content>: 120\u00a0\u00b1\u00a09;<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>104\u00a0\u00b1\u00a011\u00a0mL\u00a0min<jats:sup>\u22121<\/jats:sup>\u00a0L<jats:sup>\u22121<\/jats:sup>). A comparison of \u2206<jats:styled-content style=\"fixed-case\">LBF<\/jats:styled-content>in the passively moved and stationary leg, to partition the contribution of the blood flow response, implied that 35% of the hyperaemia resulted from cardioacceleration in the<jats:styled-content style=\"fixed-case\">CTRL<\/jats:styled-content>, whereas all the hyperaemia appeared peripheral in origin in the<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Thus, utilizing<jats:styled-content style=\"fixed-case\">PLM<\/jats:styled-content>\u2010induced hyperaemia as marker of vascular function, it is evident that peripheral vascular impairment is not an obligatory accompaniment to a<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.12173","type":"journal-article","created":{"date-parts":[[2013,10,12]],"date-time":"2013-10-12T01:42:24Z","timestamp":1381542144000},"page":"429-439","source":"Crossref","is-referenced-by-count":35,"title":["Passive leg movement\u2010induced hyperaemia with a spinal cord lesion: evidence of preserved vascular function"],"prefix":"10.1111","volume":"210","author":[{"given":"M.","family":"Venturelli","sequence":"first","affiliation":[{"name":"Department of Neurological, Neuropsychological, Morphological and Movement Sciences University of Verona Verona Italy"},{"name":"Department of Internal Medicine Division of Geriatrics University of Utah Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Amann","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Division of Geriatrics University of Utah Salt Lake City UT USA"},{"name":"Geriatric Research, Education, and Clinical Center George E. 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D.","family":"Trinity","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Division of Geriatrics University of Utah Salt Lake City UT USA"},{"name":"Geriatric Research, Education, and Clinical Center George E. Whalen VA Medical Center Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. S.","family":"Fjeldstad","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Division of Geriatrics University of Utah Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. J.","family":"Ives","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Division of Geriatrics University of Utah Salt Lake City UT USA"},{"name":"Geriatric Research, Education, and Clinical Center George E. 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