Evidence map›Paper›PMID 25759514›Full record

ArticleJournal of clinical biochemistry and nutrition2015

Contribution of nitrergic nerve in canine gingival reactive hyperemia.

Shigeru Shimada, Kazuo Todoki, Yoichi Omori, Toshizo Toyama, Masato Matsuo, Satoko Wada-Takahashi, Shun-Suke Takahashi, Masaichi-Chang-Il Lee

Open access · diamondAbstract read
In one paragraph

Article in Journal of clinical biochemistry and nutrition, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Autonomic cardiovascular changes during reactive hyperemia.Clinical physiology and functional imaging · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Shigeru ShimadaDepartment of Oral Science, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan.
Kazuo TodokiDepartment of Nursing, Junior College, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan.
Yoichi OmoriDepartment of Oral Science, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan.
Toshizo ToyamaDepartment of Infection Control, Division of Microbiology, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan.
Masato MatsuoDepartment of Tissue-Engineering, Institute for Frontier Oral Science, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan.
Satoko Wada-TakahashiDepartment of Oral Science, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan.
Shun-Suke TakahashiDepartment of Oral Science, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan.
Masaichi-Chang-Il LeeYokosuka-Shonan Disaster Health Emergency Research Center & ESR Laboratories, Graduate School of Dentistry, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan.
Kanagawa Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

gingivanitrergic nervenitric oxidereactive hyperemia

Identifiers

PMID25759514
PMCPMC4345180
OpenAlexW2021305324

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.