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DOI 10.1016/s0165-1838(96)00127-0

Медицинская библиотека · Journal of the autonomic nervous system · 1997

Skin blood flow abnormalities in a rat model of neuropathic pain: result of decreased sympathetic vasoconstrictor outflow?

Kurvers H A, Tangelder G J, De Mey J G, Slaaf D W, Beuk R J, van den Wildenberg F A, Kitslaar P J, Reneman R S, Jacobs M J

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Loose ligation of a sciatic nerve in rats provokes signs and symptoms like those observed in human conditions of neuropathic pain. Some of these have been associated with sympathetic dysfunction. Since the skin microcirculation in the rat is strongly influenced by sympathetic tone, abnormalities in skin blood flow may be used as an indirect measure of sympathetic dysfunction. We measured, by means of laser Doppler flowmetry, skin blood flow at the plantar surface of the rat hind paw before and after ipsilateral loose sciatic nerve ligation. We assessed basal skin blood flow as well as the vasoconstrictor response which follows cooling of the rat abdomen. The effectiveness of this response may be used as a measure of sympathetic vasoconstrictor outflow. As compared to the values obtained before ligation (= 100%): (1) the vasoconstrictor response was impaired (65%, P < 0.01) from day 1 onwards, whereas (2) basal skin blood flow was increased (171%; P < 0.01) from day 3 until day 5, and decreased (51%, P < 0.0001) from day 7 until day 28. At day 28, blockade of impulse propagation in the loosely ligated sciatic nerve (by means of lidocaine) did not increase the lowered level of skin blood flow. These findings suggest that in the chronic construction injury model loose ligation of a sciatic nerve reduces sympathetic vasoconstrictor outflow, which, in turn may induce supersensitivity of skin microvessels to catecholamines.

Для цитирования: Kurvers H A, Tangelder G J, De Mey J G, Slaaf D W, Beuk R J, van den Wildenberg F A, Kitslaar P J, Reneman R S, Jacobs M J. Skin blood flow abnormalities in a rat model of neuropathic pain: result of decreased sympathetic vasoconstrictor outflow?. Journal of the autonomic nervous system. 1997. DOI: 10.1016/s0165-1838(96)00127-0.

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