Vasoconstrictor reserve in neurally mediated syncope

Schondorf, Ronald; Wieling, Wouter

doi:10.1007/bf02279891

Cited by 29 publications

(27 citation statements)

References 36 publications

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“…The panel did not consider an extensive review of pathophysiology as one of the goals of the consensus process. Excellent reviews are available [94][95][96][97] .…”

Section: Tilt Testing Backgroundmentioning

confidence: 99%

Guidelines on management (diagnosis and treatment) of syncope

Brignole¹,

Alboni²,

Benditt

et al. 2001

European Heart Journal

678

432

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“…The panel did not consider an extensive review of pathophysiology as one of the goals of the consensus process. Excellent reviews are available [94][95][96][97] .…”

Section: Tilt Testing Backgroundmentioning

confidence: 99%

Guidelines on management (diagnosis and treatment) of syncope

Brignole¹,

Alboni²,

Benditt

et al. 2001

European Heart Journal

678

432

View full text Add to dashboard Cite

“…Thus, although not dispositive, the weight of evidence suggests that the absence of any differences between genders in norepinephrine or total peripheral resistance, which is the ultimate downstream determinant of the effect of increasing sympathetic nerve activity, argues against a physiologically meaningful impairment in vasomotor control in women. Numerous investigations have shown that the ultimate precipitant of hypotension and syncope is sympathetic withdrawal and vasodilation (10,24,25,45). Although the exact stimulus that causes this final common pathway is unknown, it has been argued that stimulation of ventricular mechanoreceptors in the setting of a small, hypercontractile heart may be one potential mechanism (26,33,37).…”

Section: Vascular Resistance Responses During Orthostatic Stress In Wmentioning

confidence: 99%

Hemodynamics of orthostatic intolerance: implications for gender differences

Arbab‐Zadeh

Perhonen

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

170

163

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Women have a greater incidence of orthostatic intolerance than men. We hypothesized that this difference is related to hemodynamic effects on regulation of cardiac filling rather than to reduced responsiveness of vascular resistance during orthostatic stress. We constructed FrankStarling curves from pulmonary capillary wedge pressure (PCWP), stroke volume (SV), and stroke index (SI) during lower body negative pressure (LBNP) and saline infusion in 10 healthy young women and 13 men. Orthostatic tolerance was determined by progressive LBNP to presyncope. LBNP tolerance was significantly lower in women than in men (626.8 Ϯ 55.0 vs. 927.7 Ϯ 53.0 mmHg ϫ min, P Ͻ 0.01). Women had steeper maximal slopes of Starling curves than men whether expressed as SV (12.5 Ϯ 2.0 vs. 7.1 Ϯ 1.5 ml/mmHg, P Ͻ 0.05) or normalized as SI (6.31 Ϯ 0.8 vs. 4.29 Ϯ 0.6 ml⅐m Ϫ2 ⅐mmHg Ϫ1 , P Ͻ 0.05). During progressive LBNP, PCWP dropped quickly at low levels, and reached a plateau at high levels of LBNP near presyncope in all subjects. SV was 35% and SI was 29% lower in women at presyncope (both P Ͻ 0.05). Coincident with the smaller SV, women had higher heart rates but similar mean arterial pressures compared with men at presyncope. Vascular resistance and plasma norepinephrine concentration were similar between genders. We conclude that lower orthostatic tolerance in women is associated with decreased cardiac filling rather than reduced responsiveness of vascular resistance during orthostatic challenges. Thus cardiac mechanics and Frank-Starling relationship may be important mechanisms underlying the gender difference in orthostatic tolerance. orthostatic hypotension; stroke volume; vascular resistance; pulmonary capillary wedge pressure; lower body negative pressure IN HUMANS, TOLERANCE TO ORTHOSTATIC stress requires the successful integration of multiple elements of cardiovascular control. Syncope may occur when there is an abnormally large postural decrease in central blood volume, cardiac filling pressure, stroke volume (SV), and cardiac output (CO), or inadequate neurohumoral reflex responses to orthostasis, primarily tachycardia and vasoconstriction (2). It has been noted that women have lower orthostatic tolerance than men (7,15,23,35,50). Specific mechanisms underlying this difference have not been totally elucidated and are probably multifactorial.One recent study (50) on astronauts suggested that the incidence of orthostatic presyncope after spaceflight was greatest in women, and this was ascribed to a combination of inherently lower resistance and relative hypoadrenergic responses. However, evidence for this conclusion was not definitive, because the results were obtained from a very small number of subjects analyzed retrospectively. Frey et al. (13,14) proposed that women might respond to orthostatic challenges with more prominent vagal withdrawal, whereas men might respond with greater sympathetic stimulation to the peripheral vasculature. This notion was supported by the observation that women demonstrated greater elevations in ...

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“…Human vasoconstrictor reserve, particularly during exercise, is complex, because it is dependent not only on the amount of available sympathetic vasoconstrictor activity but also on the amount of competing vasodilator activity that is directed to vascular beds. 14 …”

Section: Vasoconstrictor Reserve and Orthostatic Tolerancementioning

confidence: 99%

“…It is likely that the vasoconstrictor reserve significantly affects the maintenance of orthostatic tolerance. 13,14 However, these speculations have not yet been proven.…”

mentioning

confidence: 99%

Vasoconstrictor Reserve and Sympathetic Neural Control of Orthostasis

2004

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Background-We tested the hypothesis that individual variability in orthostatic tolerance is dependent on the degree of neural and vasomotor reserve available for vasoconstriction. Methods and Results-Muscle sympathetic nerve activity (MSNA) and hemodynamics were measured in 12 healthy young volunteers during 60°head-up tilt (HUT), followed by a cold pressor test (CPT) in HUT. Orthostatic tolerance was determined by progressive lower-body negative pressure (LBNP) to presyncope. The same protocols were performed randomly in normovolemic and hypovolemic conditions. We found that mean arterial pressure increased and stroke volume decreased, whereas heart rate (HR), MSNA, and total peripheral resistance (TPR) increased during HUT (all PϽ0.01). Application of the CPT in HUT did not increase HR or decrease stroke volume further but elevated mean arterial pressure (PϽ0.01) and increased MSNA and TPR in some subjects. There was a positive correlation between the time to presyncope from Ϫ50 mm Hg LBNP (equivalent to 60°HUT alone) and the changes in MSNA produced by the CPT under both conditions (rϭ0.442, Pϭ0.039). Those who had greater increases in MSNA had greater increases in TPR during the CPT and longer time to presyncope (both PϽ0.05). One subject had dramatic increases in MSNA but small increases in TPR during the CPT, which indicates a disassociation between sympathetic activity and the increase in peripheral vascular resistance. Conclusions-These results support our hypothesis and suggest that vasoconstrictor capability is a contributor to orthostatic tolerance in humans. Vasoconstrictor reserve therefore may be one mechanism underlying individual variability in orthostatic intolerance.

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Vasoconstrictor reserve in neurally mediated syncope

Cited by 29 publications

References 36 publications

Guidelines on management (diagnosis and treatment) of syncope

Guidelines on management (diagnosis and treatment) of syncope

Hemodynamics of orthostatic intolerance: implications for gender differences

Vasoconstrictor Reserve and Sympathetic Neural Control of Orthostasis

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