Modulation of the axon-reflex response to local heat by reactive oxygen species in subjects with chronic fatigue syndrome.

Local cutaneous heating causes vasodilation as an initial first peak, a nadir, and increase to plateau. Reactive oxygen species (ROS) modulate the heat plateau in healthy controls. The initial peak, due to C-fiber nociceptor-mediated axon reflexes, is blunted with local anesthetics and may serve as a surrogate for the cutaneous response to peripheral heat.

Baroreceptor unloading in postural tachycardia syndrome augments peripheral chemoreceptor sensitivity and decreases central chemoreceptor sensitivity.

While orthostatic tachycardia is the hallmark of postural tachycardia syndrome (POTS), orthostasis also initiates increased minute ventilation (Ve) and decreased end-tidal CO(2) in many patients. We hypothesized that chemoreflex sensitivity would be increased in patients with POTS. We therefore measured chemoreceptor sensitivity in 20 POTS (16 women and 4 men) and 14 healthy controls (10 women and 4 men), 16-35 yr old by exposing them to eucapneic hyperoxia (30% O(2)), eucapneic hypoxia (10% O(2)), and hypercapnic hyperoxia (30% O(2) + 5% CO(2)) while supine and during 70° head-upright tilt.

Defects in cutaneous angiotensin-converting enzyme 2 and angiotensin-(1-7) production in postural tachycardia syndrome.

Postural tachycardia syndrome (POTS) is associated with increased plasma angiotensin II (Ang II). Ang II administered in the presence of NO synthase inhibition with nitro-L-arginine (NLA) and Ang II type 1 receptor blockade with losartan produces vasodilation during local heating in controls. We tested whether this angiotensin-mediated vasodilation occurs in POTS and whether it is related to angiotensin-converting enzyme 2 (ACE2) and Ang-(1-7).

Angiotensin II type 1 receptor blockade corrects cutaneous nitric oxide deficit in postural tachycardia syndrome.

Low-flow postural tachycardia syndrome (POTS) is associated with increased plasma angiotensin II (ANG II) and reduced neuronal nitric oxide (NO), which decreases NO-dependent vasodilation. We tested whether the ANG II type 1 receptor (AT(1)R) antagonist losartan would improve NO-dependent vasodilation in POTS patients. Furthermore, if the action of ANG II is dependent on NO, then the NO synthase inhibitor nitro-L-arginine (NLA) would reverse this improvement.

Cutaneous neuronal nitric oxide is specifically decreased in postural tachycardia syndrome.

Low flow postural tachycardia syndrome (POTS), is associated with reduced nitric oxide (NO) activity assumed to be of endothelial origin. We tested the hypothesis that cutaneous microvascular neuronal NO (nNO) is impaired, rather than endothelial NO (eNO), in POTS. We performed three sets of experiments on subjects aged 22.

Reduced body mass index is associated with increased angiotensin II in young women with postural tachycardia syndrome.

Altered peripheral haemodynamics, decreased cardiac output, decreased blood volume and increased AngII (angiotensin II) have been reported in POTS (postural tachycardia syndrome). Recent findings indicate that BMI (body mass index) may be reduced. In the present study, we investigated the hypothesis that reduced BMI is associated with haemodynamic abnormalities in POTS and that this is related to AngII.

Cyclooxygenase and nitric oxide synthase dependence of cutaneous reactive hyperemia in humans.

We tested the hypothesis that cyclooxygenases (COXs) or COX products inhibit nitric oxide (NO) synthesis and thereby mask potential effects of NO on reactive hyperemia in the cutaneous circulation. We performed laser-Doppler flowmetry (LDF) with intradermal microdialysis in 12 healthy volunteers aged 19-25 yr. LDF was expressed as the percent cutaneous vascular conduction (%CVC) or as the maximum %CVC (%CVC(max)) where CVC is LDF/mean arterial pressure.

Increased plasma angiotensin II in postural tachycardia syndrome (POTS) is related to reduced blood flow and blood volume.

POTS (postural tachycardia syndrome) is associated with low blood volume and reduced renin and aldosterone; however, the role of Ang (angiotensin) II has not been investigated. Previous studies have suggested that a subset of POTS patients with increased vasoconstriction related to decreased bioavailable NO (nitric oxide) have decreased blood volume. Ang II reduces bioavailable NO and is integral to the renin-Ang system.

Relation of postural vasovagal syncope to splanchnic hypervolemia in adolescents.

Background: The mechanisms of simple faint remain elusive. We propose that postural fainting is related to excessive thoracic hypovolemia and splanchnic hypervolemia during orthostasis compared with healthy subjects.

Methods And Results: We studied 34 patients 12 to 22 years old referred for multiple episodes of postural faint and 11 healthy subjects.

Plantar vibration improves leg fluid flow in perimenopausal women.

Recent studies have indicated that plantar-based vibration may be an effective approach for the prevention and treatment of osteoporosis. We addressed the hypothesis of whether the plantar vibration operated by way of the skeletal muscle pump, resulting in enhanced blood and fluid flow to the lower body. We combined plantar stimulation with upright tilt table testing in 18 women aged 46-63 yr.

Noninvasive interrogation of microvasculature for signs of endothelial dysfunction in patients with chronic renal failure.

Endothelial cell dysfunction (ECD) has been demonstrated in patients with end-stage renal disease (ESRD) who have cardiovascular disease (CD) or diabetes mellitus (DM). While techniques to examine conduit arteries have been adapted to these patients, evaluation of microvascular function has lagged behind. Therefore, we used laser Doppler flowmetry (LDF) and scanned laser Doppler imaging (LDI) to quantify parameters of the postocclusion reactive hyperemia and thermal hyperemic responses (local heating to 43 degrees C) in ESRD patients (n=63) and healthy individuals (n=33).

Decreased skeletal muscle pump activity in patients with postural tachycardia syndrome and low peripheral blood flow.

Standing translocates thoracic blood volume into the dependent body. The skeletal muscle pump participates in preventing orthostatic intolerance by enhancing venous return. We investigated the hypothesis that skeletal muscle pump function is impaired in postural tachycardia (POTS) associated with low calf blood flow (low-flow POTS) and depends in general on muscle blood flow.

Local vascular responses affecting blood flow in postural tachycardia syndrome.

Postural tachycardia syndrome (POTS) is defined by orthostatic intolerance associated with abnormal upright tachycardia. Some patients have defective peripheral vasoconstriction and increased calf blood flow. Others have increased peripheral arterial resistance and decreased blood flow.

Transient orthostatic hypotension is common in adolescents.

Objectives: We hypothesized that transient hypotension associated with the symptom of lightheadedness with standing is a common phenomenon in healthy adolescents but may be mistaken for orthostatic intolerance.

Study Design: We studied 23 healthy adolescents, combining upright tilt to 70 degrees and to 35 degrees (in 12 patients) with continuous heart rate and blood pressure (BP) measurements. We measured peripheral blood flow and venous pressure in the arms and legs by using venous plethysmography.

Orthostatic hypotension in pediatrics.

Transient orthostatic hypotension is a common experience of many healthy adolescents and is the expected outcome of relatively dilated-dependent vascular tone. These children may experience brief symptoms of orthostatic intolerance when standing up rapidly, but they have no chronic symptoms or diseases. However, persistent orthostatic hypotension and chronic symptoms of orthostatic intolerance indicate postural tachycardia syndrome.

Orthostasis fails to produce active limb venoconstriction in adolescents.

Orthostasis is characterized by translocation of blood from the upper body and thorax into dependent venous structures. Although active splanchnic venoconstriction is known to occur, active limb venoconstriction remains controversial. Based on prior work, we initially hypothesized that active venoconstriction does occur in the extremities during orthostasis in response to baroreflex activation.

Inappropriate early hypotension in adolescents: a form of chronic orthostatic intolerance with defective dependent vasoconstriction.

Instantaneous orthostatic hypotension (INOH) has been reported in children and adolescents as a new entity of orthostatic intolerance in children who underwent rapid standing as an orthostatic stress test. Children with INOH were discovered among patients presenting with symptoms of chronic orthostatic intolerance, which is often related to orthostatic tachycardia. We used head-up tilt table testing at 70 degrees to investigate children presenting with symptoms of chronic orthostatic intolerance.

The relation between lower limb pooling and blood flow during orthostasis in the postural orthostatic tachycardia syndrome of adolescents.

Objectives: Postural orthostatic tachycardia syndrome (POTS) is characterized by symptoms of lightheadedness, fatigue, and signs of edema, acrocyanosis, and exaggerated tachycardia within 10 minutes of upright posture. Our objective was to determine how vascular properties contribute to the pathophysiology of POTS in adolescents.

Study Design: We compared 11 patients aged 13 to 18 years with 8 members of a control group, recording continuous heart rate and blood pressure and using strain-gauge plethysmography to measure forearm and calf blood flow and to estimate venous pressure while the subjects were supine.

Vascular perturbations in the chronic orthostatic intolerance of the postural orthostatic tachycardia syndrome.

Chronic orthostatic intolerance is often related to the postural orthostatic tachycardia syndrome (POTS). POTS is characterized by upright tachycardia. Understanding of its pathophysiology remains incomplete, but edema and acrocyanosis of the lower extremities occur frequently.

Autonomic nervous system dysfunction in adolescents with postural orthostatic tachycardia syndrome and chronic fatigue syndrome is characterized by attenuated vagal baroreflex and potentiated sympathetic vasomotion.

The objective was to determine the nature of autonomic and vasomotor changes in adolescent patients with orthostatic tachycardia associated with the chronic fatigue syndrome (CFS) and the postural orthostatic tachycardia syndrome (POTS). Continuous electrocardiography and arterial tonometry was used to investigate the heart rate and blood pressure responses before and 3-5 min after head-up tilt in 22 adolescents with POTS and 14 adolescents with CFS, compared with control subjects comprising 10 healthy adolescents and 20 patients with simple faint. Heart rate and blood pressure variability, determined baroreceptor function using transfer function analysis, and measured cardiac vagal and adrenergic autonomic responses were calculated using timed breathing and the quantitative Valsalva maneuver.