Skin Microcirculation during Tapwater Iontophoresis in Humans: Cathode Stimulates More Than Anode

Berliner, M.

doi:10.1006/mvre.1997.2025

Cited by 49 publications

(52 citation statements)

References 13 publications

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Section: Resultssupporting

confidence: 92%

“…The results were compared using RMA. Iontophoresis with normal saline consistently produced hyperemia that was approximately 20% of that produced by iontophoresis with ACh, which agrees with previously published data [15,16].A total of 97 subjects were enrolled in the study: 36 acute KS (Illness days 4-14, 4 patients were studied before receiving IVIG), 27 convalescent KS (36 days to 11 years postacute disease; median: 30 months), and 34 normal controls (Table 2). Age ranges and percent of subjects sedated with chloral hydrate were similar across all three groups.…”

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confidence: 87%

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Noninvasive Determination of Endothelial Cell Function in the Microcirculation in Kawasaki Syndrome

et al. 2007

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The aim of the study was to noninvasively assess endothelial cell (EC) function in the microcirculation using laser Doppler fluximetry (LDF) in acute and convalescent Kawasaki syndrome (KS) patients and healthy controls. KS is an acute, self-limited vasculitis of childhood that affects the EC of medium-sized arteries. No studies have addressed EC function in the peripheral microcirculation. LDF preacetylcholine and postacetylcholine (ACh) iontophoresis estimates microcirculation EC nitric oxide production leading to smooth muscle relaxation and vasodilatation, which are blunted in EC dysfunction. We studied a total of 97 subjects: 36 acute and 27 convalescent KS patients and 34 normal children. Change in blood flow was measured by LDF for 10 min postACh iontophoresis. Acute KS patients had significantly lower average flux when compared to convalescent KS patients and controls in the first 5 min postiontophoresis. However, there was no difference in flux or area under the curve (AUC) between convalescent KS patients and healthy controls. Despite a reduced response of the microvascular EC to ACh in acute KS patients, convalescent patients with and without coronary aneurysms had microvascular EC function similar to normal controls. This suggests that the EC injury in KS is confined to the endothelium of mediumsized arteries and that microvascular EC function is normal after acute KS. KeywordsCoronary artery aneurysm; Vasculitis; Pediatric heart disease Correspondence to: Jane C. Burns, jcburns@ucsd.edu. [12]. The result of these assumptions is an average flux in the area of interest that can be measured before and after iontophoresis of ACh. This technique has been used in the past to study adults with conditions known to affect the microcirculation such as diabetes. To study the ability of the endothelium to release nitric oxide, LDF is coupled with ACh iontophoresis to produce vascular smooth muscle relaxation in response to nitric oxide. The resultant vasodilation can be measured as a change in flux. Limited experience in older pediatric patients suggested that the technique might be adaptable for the study of infants and young children. We used LDF before and after ACh iontophoresis to study EC function in the microvasculature of healthy children and in children during the acute and convalescent stages of KS. Materials and Methods PatientsThree populations of subjects were studied: acute and convalescent KS patients and healthy pediatric controls. Acute KS patients were studied during their admission to the hospital for treatment with IVIG and high-dose ASA. Acute patients were studied when their rectal or oral temperature was less than 100.4°F so that elevated body temperature would not complicate the interpretation of the study. Patients older than 3 years of age who were able to cooperate with the study were evaluated without sedation. The remaining acute KS patients were studied by LDF after receiving chloral hydrate sedation for echocardiograms that were performed either during or shortly after IV...

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Section: Resultssupporting

confidence: 92%

supporting

confidence: 87%

Noninvasive Determination of Endothelial Cell Function in the Microcirculation in Kawasaki Syndrome

et al. 2007

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“…47 This is particularly problematic for iontophoresis at a cathode 48 and is dependent on the magnitude of the current and on subject age. Thus, we strove wherever possible to limit the amount of current and to use anodal agents wherever possible.…”

Section: Limitationsmentioning

confidence: 99%

Decreased Microvascular Nitric Oxide–Dependent Vasodilation in Postural Tachycardia Syndrome

2005

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Background-One variant of postural tachycardia syndrome (POTS), designated low-flow POTS, is associated with decreased peripheral blood flow related to impaired local vascular regulation. Methods and Results-To investigate the hypothesis that microvascular endothelial dysfunction produces decreased peripheral blood flow in low-flow POTS, we performed experiments using laser-Doppler flowmetry (LDF) combined with iontophoresis in 15 low-flow POTS patients, 17 normal-flow POTS patients, and 13 healthy reference volunteers varying in age from 14 to 22 years. We tested whether ␣-adrenergic vasoregulation was impaired using iontophoretic delivery of tyramine, phentolamine, and bretylium followed by a norepinephrine dose response. We tested endothelial-dependent and -independent receptor-mediated vasodilation by measuring acetylcholine and sodium nitroprusside dose responses. We tested whether nitric oxide-dependent vasodilation was different in these groups by testing the local thermal hyperemic response to saline used as a reference compared with the nitric oxide synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME). Adrenergic and receptor-dependent cutaneous vasoregulation was similar for low-flow POTS, normal-flow POTS, and reference subjects. Thermal hyperemia produced distinctly different findings: there was marked attenuation of the nitric oxide-sensitive plateau during prolonged heating, which was insensitive to L-NAME in low-flow POTS subjects. The pattern of thermal hyperemia response in low-flow POTS subjects during saline administration resembled the pattern in reference subjects during L-NAME administration and was minimally affected by L-NAME. Conclusions-The

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“…22]] following nociceptor activation is involved in the current-induced vasodilation attending iontophoresis [6, 23], either by a direct or indirect activation of nociceptors. Among the possible indirect mechanisms of nociceptor activation is a progressive local pH change, which would result from current application [24]and which could stimulate the nociceptors.…”

Section: Introductionmentioning

confidence: 99%

Current-Induced Vasodilation during Water Iontophoresis (5 min, 0.10 mA) Is Delayed from Current Onset and Involves Aspirin Sensitive Mechanisms

et al. 2002

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Study of the microcirculation by iontophoresis is potentially confounded by any non-specific effects of current application. Laser Doppler flow (LDF, mean ± SD; arbitrary units; AU) was recorded on the forearms of healthy volunteers during and 20 min following application of 0.10-mA current for 1, 3 and 5 min, using deionised water as a vehicle. Local heating to 44°C was then applied for 24 min to assess maximal vasodilation. Cathodal current applications resulted in delayed and prolonged vasodilation (peak values: 78 ± 29, 75 ± 19, 80 ± 37 AU) whereas anodal peak LDF was 13 ± 6, 27 ± 34 and 72 ± 40 AU for 1-, 3- and 5-min periods of current applications, respectively. From current onset, inflexion points in the responses to 3- and 5-min anodal current applications occurred at 4.5 and 6.5 min, respectively, and at ∼1.5 min for all cathodal current applications. For 5-min current applications: a preliminary tourniquet ischaemia neither changed the time course nor the amplitude of the response to current application. In this situation, local anaesthesia abolished the current-induced vasodilation. Chronic capsaicin pretreatment decreased the amplitude of the vasodilation. Pretreatment with 500 mg oral aspirin decreased the cathodal vasodilation and abolished the anodal vasodilation, even in the absence of preliminary ischaemia. We conclude that vasodilation to prolonged application of 0.10-mA continuous monopolar current after transient tourniquet ischaemia cannot be exclusively the result of an axon reflex initiated by current onset. This current-induced vasodilation is at least partly dependent on capsaicin-sensitive afferent fibres and relies on aspirin-sensitive mechanisms at both polarities.

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Skin Microcirculation during Tapwater Iontophoresis in Humans: Cathode Stimulates More Than Anode

Cited by 49 publications

References 13 publications

Noninvasive Determination of Endothelial Cell Function in the Microcirculation in Kawasaki Syndrome

Noninvasive Determination of Endothelial Cell Function in the Microcirculation in Kawasaki Syndrome

Decreased Microvascular Nitric Oxide–Dependent Vasodilation in Postural Tachycardia Syndrome

Current-Induced Vasodilation during Water Iontophoresis (5 min, 0.10 mA) Is Delayed from Current Onset and Involves Aspirin Sensitive Mechanisms

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