| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
Endotoxin administration to the rat induces various pathophysiological reactions including changes in PAF(platelet-activating factor)and arachidonate metabolisms in different tissues. We investigated the effect of endotoxin administered systemically on prostagiandin(PG)l_2 and thromboxane(TX)A_2 production in dental pulp tissue in the rat. Intravenous administration of endotoxin induced an increase in both PGl_2 and TXA_2 production in a dose- and time-dependent manner. This effect of endotoxin was not prevented by the pretreatment of PAF antagonist, and was not accompanied by the increase of PAF content in the pulp tissue. Endotoxin had no direct effect on PG and TX production when incubated in vitro with isolated pulp tissues. On the other hand, endotoxin treatment caused an increase only in TXA_2 production by the lung tissue, and had no effect in the intestinal tissue, suggesting that arachidonate metabolism in the pulp tissue is more susceptible to endotoxic shock than in these ti
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ssues. Despite the increase in PG and TX production, endotoxin injection did not cause an increase in vascular permeability in the pulp tissue. However, interestingly, preliminary experiment showed that endotoxin caused a disturbance of dentin formation. The precise mechanisms of effects of endotoxin administration on pulpal arachidonate metabolism and dentin formation remain to be clarified. We also investigated the role of PAF in cell-cell interaction among leukocytes, platelets and endothelial cells, and revealed that PAF induced platelet adhesion to endothelial cell surface when leukocytes were coincubated in vitro, suggesting that such an interaction may play an important role in pathogeheisis of microcirculation disturbance. Thus, the present study indicates that arachidonate metabolism in the pulp tissue can be altered by systematically administered agent, and suggests that this is an useful model for studying the role of arachidonate metagolitbs in pathophysioldgy of the dental pulp injury. Less
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