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      Anodal Current Intensities above 40 μA Interfere with Current-Induced Axon-Reflex Vasodilatation in Human Skin


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          When using iontophoresis, the ‘non-specific’ vasodilatation (NSV) that is observed as a result of C-fibre excitation is generally attributed to the local accumulation of protons under the anode. NSV following prolonged 100-µA anodal current application only appears after the current is stopped. Break excitation alone does not explain the delayed onset of this vasodilatation. We hypothesised that this delay could result from an anodal block and thus, that a minimal intensity would be required to achieve hyperpolarisation of primary afferent fibres (mainly C-fibres). Using laser Doppler flowmetry, cutaneous blood flow was recorded in the forearms of 8 healthy volunteers 2 min before current application, during the application and 20 min after stopping the monopolar anodal current. In protocol 1, after 2.5 min of current application at an intensity of 100 µA, the intensity was abruptly decreased to 0–80 µA for a second 2.5-min period. The onset of vasodilatation was only delayed at intensities >30 µA during this second period. In protocol 2, re-application of the current after a 50-second interruption (expected to allow for the occurrence of an axon reflex) did not interfere with the onset of vasodilatation. Thus: (1) the minimal intensity interfering with the axon reflex is far lower than that reported for C-fibre blockade in isolated nerves; (2) the results suggest that current application does not directly interfere with the vasodilator mechanisms induced by the axon reflex at the level of smooth muscle cells.

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          Most cited references 7

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          Functional roles of KATP channels in vascular smooth muscle.

          1. ATP-sensitive potassium channels (K(ATP)) are present in vascular smooth muscle cells and play important roles in the vascular responses to a variety of pharmacological and endogenous vasodilators. 2. The K(ATP) channels are composed of four inwardly rectifying K+ channel subunits and four regulatory sulphonylurea receptors. The K(ATP) channels are inhibited by intracellular ATP and by sulphonylurea agents. 3. Pharmacological vasodilators such as cromakalim, pinacidil and diazoxide directly activate K(ATP) channels. The associated membrane hyperpolarization closes voltage-dependent Ca2+ channels, which leads to a reduction in intracellular Ca2+ and vasodilation. 4. Endogenous vasodilators such as calcitonin gene-related peptide, vasoactive intestinal polypeptide, prostacylin and adenosine activate K(ATP) by stimulating the formation of cAMP and increasing the activity of protein kinase A. Part of the mechanism of contraction of endogenous vasoconstrictors is due to inhibition of K(ATP) channels. 5. The K(ATP) channels appear to be tonically active in some vascular beds and contribute to the physiological regulation of vascular tone and blood flow. These channels also are activated under pathophysiological conditions, such as hypoxia, ischaemia, acidosis and septic shock, and, in these disease states, may play an important role in the regulation of tissue perfusion.
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            Cutaneous vasodilation induced by local warming, sodium nitroprusside, and bretylium iontophoresis on the hand.

            Local warming alone induces a cutaneous vasodilation considered as maximal. The argument that local warming generates a maximum flow is being tested by vasodilation with alternate approaches to see if a greater vasodilation is possible: blockade of the release of transmitters from the adrenergic nerve endings with bretylium tosylate or direct pharmacological action on vascular smooth muscle using sodium nitroprusside. Nine healthy subjects participated in two experiments in which SkBF was measured simultaneously by laser Doppler flowmetry on the dorsal aspects of both hands. In the first protocol the vasodilator effects of 20 min of local warming at 44 degreesC were measured on one hand and the effects of iontophoresis of sodium nitroprusside on the other. The second protocol was like the first except that iontophoresis of bretylium tosylate instead of sodium nitroprusside was performed. Local warming induced an increase of SkBF from 17.6 +/- 4.4 to 140.2 +/- 33.2 AU (P < 0.01) while it rose from 16.7 +/- 4.0 to 114.7 +/- 11.0 AU (P < 0.001) during sodium nitroprusside iontophoresis. During the second protocol local warming induced an increase of SkBF from 14.9 +/- 2.1 to 117.7 +/- 25.4 AU (P < 0.01) while it rose from 19.6 +/- 2.6 to 120.5 +/- 11.3 AU (P < 0.001) during bretylium iontophoresis. However, in both experiments, the increase of SkBF attained during iontophoresis did not differ significantly from the increase achieved by local warming. We conclude that the effects of iontophoresis of sodium nitroprusside or of bretylium produce a cutaneous vasodilation as high as a local warming on the dorsal aspect of the hand. Copyright 1998 Academic Press.
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              Current-Induced Vasodilation during Water Iontophoresis (5 min, 0.10 mA) Is Delayed from Current Onset and Involves Aspirin Sensitive Mechanisms

               S Durand,  B Fromy,  P Bouyé (2002)
              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.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                June 2004
                30 June 2004
                : 41
                : 3
                : 261-267
                CNRS UMR 6188, Laboratory of Physiology, University Hospital, Angers, France
                78665 J Vasc Res 2004;41:261–267
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 1, References: 31, Pages: 7
                Research Paper


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