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Contribution of nitrergic nerve in canine gingival reactive hyperemia
Reactive hyperemia reflects a compensatory vasodilation response of the local vasculature in ischemic tissue. The purpose of this study is to clarify the mechanism of regulation of this response in gingival circulation by using pharmacological analysis of reactive hyperemia and histochemical analysi...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
the Society for Free Radical Research Japan
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4345180/ https://www.ncbi.nlm.nih.gov/pubmed/25759514 http://dx.doi.org/10.3164/jcbn.14-71 |
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author | Shimada, Shigeru Todoki, Kazuo Omori, Yoichi Toyama, Toshizo Matsuo, Masato Wada-Takahashi, Satoko Takahashi, Shun-suke Lee, Masaichi-Chang-il |
author_facet | Shimada, Shigeru Todoki, Kazuo Omori, Yoichi Toyama, Toshizo Matsuo, Masato Wada-Takahashi, Satoko Takahashi, Shun-suke Lee, Masaichi-Chang-il |
author_sort | Shimada, Shigeru |
collection | PubMed |
description | Reactive hyperemia reflects a compensatory vasodilation response of the local vasculature in ischemic tissue. The purpose of this study is to clarify the mechanism of regulation of this response in gingival circulation by using pharmacological analysis of reactive hyperemia and histochemical analysis of gingival tissue. Application of pressure to the gingiva was used to create temporary ischemia, and gingival blood flow was measured after pressure release. Reactive hyperemia increased in proportion to the duration of pressure. Systemic hemodynamics remained unaffected by the stimulus; therefore, the gingival reactive hyperemia reflected a local adjustment in circulation. Gingival reactive hyperemia was significantly suppressed by nitric oxide (NO) synthase inhibitors, especially the neural NO synthase-selective antagonist 7-nitroindazole, but not by anticholinergic drugs, β-blockers, or antihistaminergic drugs. Moreover, immunohistochemical staining for neural NO synthase and histochemical staining for NADPH diaphorase activity were both positive in the gingival perivascular region. These histochemical and pharmacological analyses show that reactive hyperemia following pressure release is mediated by NO-induced vasodilation. Furthermore, histochemical analysis strongly suggests that NO originates from nitrergic nerves. Therefore, NO may play an important role in the neural regulation of local circulation in gingival tissue ischemia. |
format | Online Article Text |
id | pubmed-4345180 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | the Society for Free Radical Research Japan |
record_format | MEDLINE/PubMed |
spelling | pubmed-43451802015-04-09 Contribution of nitrergic nerve in canine gingival reactive hyperemia Shimada, Shigeru Todoki, Kazuo Omori, Yoichi Toyama, Toshizo Matsuo, Masato Wada-Takahashi, Satoko Takahashi, Shun-suke Lee, Masaichi-Chang-il J Clin Biochem Nutr Original Article Reactive hyperemia reflects a compensatory vasodilation response of the local vasculature in ischemic tissue. The purpose of this study is to clarify the mechanism of regulation of this response in gingival circulation by using pharmacological analysis of reactive hyperemia and histochemical analysis of gingival tissue. Application of pressure to the gingiva was used to create temporary ischemia, and gingival blood flow was measured after pressure release. Reactive hyperemia increased in proportion to the duration of pressure. Systemic hemodynamics remained unaffected by the stimulus; therefore, the gingival reactive hyperemia reflected a local adjustment in circulation. Gingival reactive hyperemia was significantly suppressed by nitric oxide (NO) synthase inhibitors, especially the neural NO synthase-selective antagonist 7-nitroindazole, but not by anticholinergic drugs, β-blockers, or antihistaminergic drugs. Moreover, immunohistochemical staining for neural NO synthase and histochemical staining for NADPH diaphorase activity were both positive in the gingival perivascular region. These histochemical and pharmacological analyses show that reactive hyperemia following pressure release is mediated by NO-induced vasodilation. Furthermore, histochemical analysis strongly suggests that NO originates from nitrergic nerves. Therefore, NO may play an important role in the neural regulation of local circulation in gingival tissue ischemia. the Society for Free Radical Research Japan 2015-03 2015-03-01 /pmc/articles/PMC4345180/ /pubmed/25759514 http://dx.doi.org/10.3164/jcbn.14-71 Text en Copyright © 2015 JCBN This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Shimada, Shigeru Todoki, Kazuo Omori, Yoichi Toyama, Toshizo Matsuo, Masato Wada-Takahashi, Satoko Takahashi, Shun-suke Lee, Masaichi-Chang-il Contribution of nitrergic nerve in canine gingival reactive hyperemia |
title | Contribution of nitrergic nerve in canine gingival reactive hyperemia |
title_full | Contribution of nitrergic nerve in canine gingival reactive hyperemia |
title_fullStr | Contribution of nitrergic nerve in canine gingival reactive hyperemia |
title_full_unstemmed | Contribution of nitrergic nerve in canine gingival reactive hyperemia |
title_short | Contribution of nitrergic nerve in canine gingival reactive hyperemia |
title_sort | contribution of nitrergic nerve in canine gingival reactive hyperemia |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4345180/ https://www.ncbi.nlm.nih.gov/pubmed/25759514 http://dx.doi.org/10.3164/jcbn.14-71 |
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