Regional blood volume and peripheral blood flow in postural tachycardia syndrome

Stewart, Julian M.; Montgomery, Leslie D.

doi:10.1152/ajpheart.00086.2004

Cited by 91 publications

(111 citation statements)

References 34 publications

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“…Pelvic impedance was measured using a Minnesota Impedance Cardiograph (Instrumentation for Medicine, Greenwich, CT). Pairs of electrocardiogram electrodes were placed at the xyphoid and iliac crest on both sides of the body (33). A constant alternating current of 4 mA at 100 kHz was passed through the pelvic region between the outer electrodes.…”

Section: Methodsmentioning

confidence: 99%

Cardiovascular responses to lower body negative pressure before and after 4 h of head-down bed rest and seated control in men and women

Edgell

Grinberg

Gagné

et al. 2012

Journal of Applied Physiology

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Edgell H, Grinberg A, Gagné N, Beavers KR, Hughson RL. Cardiovascular responses to lower body negative pressure before and after 4 h of head-down bed rest and seated control in men and women. J Appl Physiol 113: 1604 -1612, 2012. First published September 13, 2012 doi:10.1152/japplphysiol.00670.2012.-Cardiovascular deconditioning after a 4-h head-down bed rest (HDBR) might be a consequence of the time of day relative to pre-HDBR testing, or simply 4 h of confinement and inactivity rather than the posture change. Ten men and 11 women were studied during lower body negative pressure (LBNP) before and after 4-h HDBR and 4-h seated posture (SEAT) as a control for time of day and physical inactivity effects to test the hypotheses that cardiovascular deconditioning was a consequence of the HDBR posture, and that women would have a greater deconditioning response. Following HDBR, men and women had lower blood volume, higher heart rate with a greater increase during LBNP, a greater decrease of stroke volume during LBNP, lower central venous pressure, smaller inferior vena cava diameter, higher portal vein resistance index with a greater increase during LBNP, but lower forearm vascular resistance, lower norepinephrine, and lower renin. Women had lower vasopressin and men had higher vasopressin after HDBR, and women had lower pelvic impedance and men higher pelvic impedance. Following SEAT, brachial vascular resistance was reduced, thoracic impedance was elevated, the reduction of central venous pressure during LBNP was changed, women had higher angiotensin II whereas men had lower levels, and pelvic impedance increased in women and decreased in men. Cardiovascular deconditioning was greater after 4-h HDBR than after SEAT. Women and men had similar responses for most cardiovascular variables in the present study that tested the responses to LBNP after short-duration HDBR compared with a control condition. cardiovascular deconditioning; orthostatic challenge; sex differences; regional blood flow HEAD-DOWN BED REST (HDBR), as short as 4 h, is used as a simulation of microgravity exposure (6, 13). The body adapts quickly to this change in posture and reveals cardiovascular deconditioning that is characterized by elevations in heart rate (HR) and altered hormonal responses during application of lower body negative pressure (LBNP; i.e., lower baseline renin and angiotensin II which increased more in response to LBNP) (13) and by dramatic reduction in tolerance to an upright tilt (6). Thus acute alterations in the normal gravitational loading of the body appear to induce changes in the normal regulation of arterial blood pressure in the upright posture (13,19,35). But whether the changes during an orthostatic challenge after 4-h HDBR are an effect of the change in gravitational loading of the cardiovascular system or simply an effect of time of day and/or confinement has not been examined.Inherent in 4-h HDBR studies is the comparison of responses at different times of day for pre-vs. post-HDBR measurements. Several studies ha...

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Section: Methodsmentioning

confidence: 99%

Cardiovascular responses to lower body negative pressure before and after 4 h of head-down bed rest and seated control in men and women

Edgell

Grinberg

Gagné

et al. 2012

Journal of Applied Physiology

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“…The decrease in cardiac output comprises a 40% decrease in stroke volume associated with reflex tachycardia, increased peripheral resistance, and a generally maintained systolic blood pressure (SBP) with somewhat reduced pulse pressure (PP) while quietly standing (35). Changes in circulatory physiology during head-up tilt (HUT) are said to resemble the changes observed during hypovolemia caused by dehydration or hemorrhage (39,41).…”

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confidence: 99%

Differential effects of lower body negative pressure and upright tilt on splanchnic blood volume

Taneja¹,

Moran²,

Medow³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Taneja I, Moran C, Medow MS, Glover JL, Montgomery LD, Stewart JM. Differential effects of lower body negative pressure and upright tilt on splanchnic blood volume. Am J Physiol Heart Circ Physiol 292: H1420 -H1426, 2007. First published November 3, 2006; doi:10.1152/ajpheart.01096.2006.-Upright posture and lower body negative pressure (LBNP) both induce reductions in central blood volume. However, regional circulatory responses to postural changes and LBNP may differ. Therefore, we studied regional blood flow and blood volume changes in 10 healthy subjects undergoing graded lower-body negative pressure (Ϫ10 to Ϫ50 mmHg) and 8 subjects undergoing incremental head-up tilt (HUT; 20°, 40°, and 70°) on separate days. We continuously measured blood pressure (BP), heart rate, and regional blood volumes and blood flows in the thoracic, splanchnic, pelvic, and leg segments by impedance plethysmography and calculated regional arterial resistances. Neither LBNP nor HUT altered systolic BP, whereas pulse pressure decreased significantly. Blood flow decreased in all segments, whereas peripheral resistances uniformly and significantly increased with both HUT and LBNP. Thoracic volume decreased while pelvic and leg volumes increased with HUT and LBNP. However, splanchnic volume changes were directionally opposite with stepwise decreases in splanchnic volume with LBNP and stepwise increases in splanchnic volume during HUT. Splanchnic emptying in LBNP models regional vascular changes during hemorrhage. Splanchnic filling may limit the ability of the splanchnic bed to respond to thoracic hypovolemia during upright posture.vasoconstriction; splanchnic; blood volume; orthostatic stress; hemorrhage STANDING TRANSLOCATES BLOOD from the central thoracic circulation to the dependent regional circulations, producing ϳ20% reduction in cardiac output. The decrease in cardiac output comprises a 40% decrease in stroke volume associated with reflex tachycardia, increased peripheral resistance, and a generally maintained systolic blood pressure (SBP) with somewhat reduced pulse pressure (PP) while quietly standing (35). Changes in circulatory physiology during head-up tilt (HUT) are said to resemble the changes observed during hypovolemia caused by dehydration or hemorrhage (39, 41).Lower body negative pressure (LBNP; see Refs. 44 -46) has been used as a reversible simulation for hemorrhage (8,30). LBNP has also been used to model orthostatic stress (7) because many of the changes of neurovascular physiology resemble changes during standing or HUT (31). Thus, for example, both HUT and LBNP produce central hypovolemia and comparable unloading of the cardiopulmonary and arterial baroreceptors (9, 19). However, gravitational differences in regional vascular properties have also been noted (21, 24). Thus recent work by Cooke et al. (8) and el Bedawi and Hainsworth (12) has demonstrated that, although LBNP physiology most closely resembles the physiology of acute hemorrhage, it may be incomplete as a model for orthostatic stress, which must prod...

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“…Many patients with POTS are so debilitated by their orthostatic symptoms, they are unable to work. 2 A number of different pathophysiologies underlie symptoms in subgroups of patients, [3][4][5][6][7][8][9][10][11][12][13][14] but the basis of POTS remains obscure in most afflicted individuals. Genes encoding the NE transporter (SLC6A2), 13 the ␤-1 15 and ␤-2 (G. Jacob, unpublished data, 2005) adrenergic receptors, and endothelin-1 (R. Winker, unpublished data, 2005) are associated with the development of POTS.…”

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confidence: 99%

Endothelial NO Synthase Polymorphisms and Postural Tachycardia Syndrome

et al. 2005

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Abstract-Postural tachycardia syndrome (POTS) is a heterogeneous disorder characterized by an excessive rise in heart rate and symptoms consistent with cerebral hypoperfusion in the upright position. NO produced by endothelial NO synthase is a significant factor in the regulation of blood flow. Genetic polymorphisms in the promoter region (T-786C) and exon 7 (E298D) of the NO synthase isoform 3 gene affect enzyme activity and have been associated with a number of cardiovascular diseases. Because some findings in POTS suggest aberrant NO-mediated functions, we postulated that the variant genotypes of these polymorphisms may increase the risk of developing POTS and correlate with more severe symptoms. We genotyped 136 patients with POTS (mean age 32.2Ϯ9.9 years; 46 men and 90 women) from Nashville, Tenn, and Vienna, Austria, and compared them with 191 healthy volunteers (mean age 29.1Ϯ8.0 years; 127 men and 64 women). Participants also underwent orthostatic testing with blood pressure, heart rate, and plasma norepinephrine measurements while supine and upright.

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Regional blood volume and peripheral blood flow in postural tachycardia syndrome

Cited by 91 publications

References 34 publications

Cardiovascular responses to lower body negative pressure before and after 4 h of head-down bed rest and seated control in men and women

Cardiovascular responses to lower body negative pressure before and after 4 h of head-down bed rest and seated control in men and women

Differential effects of lower body negative pressure and upright tilt on splanchnic blood volume

Endothelial NO Synthase Polymorphisms and Postural Tachycardia Syndrome

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