|| Checking for direct PDF access through Ovid
An analysis of nerve vascular changes in nerve roots induced by serotonin in chronically compressed nerve roots.To assess the hypotheses that serotonin might have a vasoconstrictive effect in chronically compressed nerve roots.The 5-hydroxytryptamine 2A receptor is involved in serotonin-induced activation or sensitization of sensory nerve terminals. Serotonin exerts complex effects on pain and hyperalgesia through various receptor subtypes located at various levels of the pain transmission system. Serotonin induces endothelium-dependent contraction in vascular diseases. However, there is no knowledge regarding a response of nerve vasculature induced by serotonin in chronically compressed nerve roots.A total of 45 dogs were used. A plastic balloon was placed under the lamina L7 and inflated to 10 mm Hg and left for 1 week. Four experimental groups were used: no operation (Group A, n = 15), the balloon was placed under the lamina but not inflated (Group B, n = 10), the balloon was inflated to 10 mm Hg for 1 week and the pressure was released just before the measurement (Group C, n = 10), and the balloon was inflated to 10 mm Hg for 1 week and inflation was maintained during the measurements (Group D, n = 10). The blood vessels of the second or third sacral nerve were defined after an intra-arterial injection of 0.5 μmol/L or 1.0 μmol/L serotonin using a specially designed operation microscope equipped with a video camera. In all groups 0.5 μmol/L serotonin (each group, n = 5) or 1.0 μmol/L serotonin (each group, n = 5) was injected. In Group A (n = 5) saline was injected. The measurements of diameter of observed blood vessels and blood flow index were performed on video recordings. All statistical assessments were performed by Wilcoxon signed-ranks test and Fisher’s PLSD.In Group A, the diameter of blood vessels and blood flow did not change after administration of saline. In the noncompression groups (Groups A and B) the diameter of blood vessels and blood flow increased after injection of 0.5 μmol/L serotonin. In compression groups (Groups C and D) the blood vessels contracted after injecting 0.5 μmol/L serotonin and blood flow decreased. There was a significant difference in the diameter of blood vessels and blood flow between noncompression and compression groups (P < 0.01). There was no difference regarding diameter of blood vessels between releasedcompression (Group C) and maintained compression during measurement group (Group D). In all groups blood vessels contracted and blood flow decreased after injecting 1.0 μmol/L. In electron microscopic observation tight junction of endothelial cells was destroyed in chronically compression nerve roots.The present study demonstrated that serotonin had a vasodilative effect on the intact nerve roots, whereas there was a vasoconstrictive effect to the chronically compressed nerve roots. There was no difference in the diameter of blood vessels between released compression and maintained compression during measurement group. Results suggested that dysfunction of endothelial cells induced by serotonin rather than mechanical compression itself might lead to contraction of blood vessels under chronic compression.Serotonin had a vasoconstrictive effect on the chronically compressed nerve roots.