{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T03:43:15Z","timestamp":1790912595944,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2012,3,15]],"date-time":"2012-03-15T00:00:00Z","timestamp":1331769600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2012,4,15]]},"abstract":"<jats:p><jats:bold>Key points\u2002<\/jats:bold> <jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Syncope is a common clinical condition occurring even in healthy people without manifest cardiovascular disease; we determined the role of cardiac output and sympathetic vasoconstriction in neurally mediated (pre)syncope.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Our data showed that a moderate fall in cardiac output with coincident vasodilatation occurred in the majority (64%) of the presyncopal subjects, while a marked fall in cardiac output, driven predominantly by a decrease in heart rate, with no changes in total peripheral resistance at presyncope, occurred in a smaller (36%) subset.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Sympathetic withdrawal occurred late, after the onset of hypotension.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Sympathetic vasoconstriction and baroreflex sensitivity during symptom\u2010free upright posture were well preserved and, thus, an intrinsic impairment of sympathetic neural control and vasomotor responsiveness was not the cause of neurally mediated (pre)syncope in this population.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>These results help us better understand the mechanisms for syncope in 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