title: Chronic orthostatic intolerance: a disorder with discordant cardiac and vascular sympathetic control.
abstract: BACKGROUND
  Chronic orthostatic intolerance (COI) is a debilitating autonomic condition in young adults. Its neurohumoral and hemodynamic profiles suggest possible alterations of postural sympathetic function and of baroreflex control of heart rate (HR).
  
  
  RESULTS
  In 16 COI patients and 16 healthy volunteers, intra-arterial blood pressure (BP), ECG, central venous pressure (CVP), and muscle sympathetic nerve activity (MSNA) were recorded at rest and during 75 degrees tilt. Spectral analysis of RR interval and systolic arterial pressure (SAP) variabilities provided indices of sympathovagal modulation of the sinoatrial node (ratio of low-frequency to high-frequency components, LF/HF) and of sympathetic vasomotor control (LFSAP). Baroreflex mechanisms were assessed (1) by the slope of the regression line obtained from changes of RR interval and MSNA evoked by pharmacologically induced alterations in BP and (2) by the index alpha, obtained from cross-spectral analysis of RR and SAP variabilities. At rest, HR, MSNA, LF/HF, and LFSAP were higher in COI patients, whereas BP and CVP were similar in the two groups. During tilt, BP did not change and CVP fell by the same extent in the 2 groups; the increase of HR and LF/HF was more pronounced in COI patients. Conversely, the increase of MSNA was lower in COI than in control subjects. Baroreflex sensitivity was similar in COI and control subjects at rest; tilt reduced alpha similarly in both groups.
  
  
  CONCLUSIONS
  COI is characterized by an overall enhancement of noradrenergic tone at rest and by a blunted postganglionic sympathetic response to standing, with a compensatory cardiac sympathetic overactivity. Baroreflex mechanisms maintain their functional responsiveness. These data suggest that in COI, the functional distribution of central sympathetic tone to the heart and vasculature is abnormal.
authors.affiliation: Syncope Service in the Autonomic Dysfunction Unit, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN, USA.
authors.forename: R
authors.initials: R
authors.lastname: Furlan
authors.forename: G
authors.initials: G
authors.lastname: Jacob
authors.forename: M
authors.initials: M
authors.lastname: Snell
authors.forename: D
authors.initials: D
authors.lastname: Robertson
authors.forename: A
authors.initials: A
authors.lastname: Porta
authors.forename: P
authors.initials: P
authors.lastname: Harris
authors.forename: R
authors.initials: R
authors.lastname: Mosqueda-Garcia
mesh_terms: D000328:Adult; D002908:Chronic Disease; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D011187:Posture; D011311:Pressoreceptors / Q000502:physiology; D012018:Reflex; D013564:Sympathetic Nervous System / Q000502:physiology*; D013610:Tachycardia / Q000503:physiopathology*