Contribution of nitrergic nerve in canine gingival reactive hyperemia

DOI 被引用文献4件 参考文献26件 オープンアクセス
  • Shimada Shigeru
    Department of Oral Science, Kanagawa Dental University
  • Todoki Kazuo
    Department of Nursing, Junior College, Kanagawa Dental University
  • Omori Yoichi
    Department of Oral Science, Kanagawa Dental University
  • Toyama Toshizo
    Department of Infection Control, Division of Microbiology, Kanagawa Dental University
  • Matsuo Masato
    Department of Tissue-Engineering, Institute for Frontier Oral Science, Kanagawa Dental University
  • Wada-Takahashi Satoko
    Department of Oral Science, Kanagawa Dental University
  • Takahashi Shun-suke
    Department of Oral Science, Kanagawa Dental University
  • Lee Masaichi-Chang-il
    Yokosuka-Shonan Disaster Health Emergency Research Center & ESR Laboratories, Graduate School of Dentistry, Kanagawa Dental University

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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.

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