1988 Fiscal Year Final Research Report Summary
Studies on increasing sensitivities in pulpal inflammatory reactions by new inflammatory mediator(PAF)
| Project/Area Number |
61480382
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
SANJOU Daisuke Tohoku University, School of Dentistry, Professor, 歯学部, 教授 (70013943)
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| Co-Investigator(Kenkyū-buntansha) |
OGURA YASUMI Tohoku University, School of Dentistry, Professor, 歯学部, 教授 (60091667)
HIRAFUJI Masahiko Tohoku University, School of Dentistry, Assistant, 歯学部, 助手 (20142987)
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| Project Period (FY) |
1986 – 1988
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| Keywords | inflammatory mediators / PAF / platelet aggregation / vascular contraction / inflammation of the pulp / adrenaline / pulmonary respiration resistance / 抗アレルギー薬 |
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| Research Abstract |
Some stimulants evoke easily an inflammatory reactionin the pulp tissue. We have reported that histamine and other inflammatory muediators were detected in the pulp and that may be play a role in the inflammatory process. PAF. a new inflammatory mediator, was studied on the signification in pulpal inflammation.
1. PAF was detected in pulpal tissue of rats. And PAF stimulated PGI_2>TXA_2 release from rat pulppal tissue. The fact suggests that the endothelial celles play a important role.
2. In the arterial smooth muscle, PAF potentiated the contracted reaction toadrenaline. The potentiation was not found in other smooth muscles.
3. In neuronal inflammation ( reciprocal electrical stimulation experiments in the sciatic nerve), PAF did not potentiate the reaction, and it increased thecapillary permeability under the existence of endothelial cells. This also is supported by the fact that in the in vivo nerve-muscle preparation, the relaxant action to anticurare agents is inhibited by pretreatment of PAF.
4. In pulmonary respirationresistance experiments, the increase of tracheal contraction with PAF was antagonized by anti-PAF drugs, and also anti- allergic agents and B_1 related compounds. The pulatelet aggregating activity, howoevor, did not be influenced by theseantagonists. Therefore, the above mentionned results suggest that in the initial inflammatory process in the pulpal tissue, PAF may be play a role of the formation of the prearrangements of inflammatory conditions and that the PAF -induced condition may be very intensify the release and actions of mediators.
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