STUDIES ON THE MECHANISM OF ENDOTOXIN-INDUCED MICROIRCULATORY DISTURBANCE IN DENTAL PULP TUSSUE

本研究旨在探讨内毒素对大鼠牙髓组织损伤的影响，并从药理学和组织学角度阐明其作用机制。大鼠静脉注射大肠杆菌0111：B4的脂多糖-由于内毒素对肺和肠组织无影响，牙髓比肠组织更易受到内毒素休克的影响。牙髓组织中脂质过氧化物的增加可归因于牙髓组织中的缺血性损伤或白细胞浸润。用HPLC法分析内毒素处理的大鼠牙髓组织中腺嘌呤核苷酸含量，发现AMP明显升高，ATP明显降低。组织学观察显示内毒素可引起牙髓细胞核变形。然而，未观察到炎症反应，如白细胞浸润或血管舒张。这些结果表明，内毒素全身给药大鼠诱导牙髓缺血性组织损伤。本研究还探讨了白细胞诱导血小板与内皮细胞粘附的机制。结果表明，血小板粘附伴随着血小板cGMP的减少，而不是cAMP的产生部分参与了白细胞诱导的血小板粘附机制。

The aim of the present research project was to investigate the effect of systemic administration of endotoxin on the tissue injury of rat dental pulp, and to clarify its mechanism by pharmaclogical and histological studies. The intravenous advinistration of ecdotoxin (lipopolysaccharide of E.coli 0111 : B4) to the rat caused an increase in the cantent of lipid peroxides in the dental pilp, suggesting that endotoxin induced the microcirculatory disturbance. Since endotosin had no effect in the lung and intestinal tissues, dental pulp was more susceptible to endotoxic shock tan tese tissues. The increase of lipid peroxides in the pulp tissue was attributable to ischemic injury or leulocyte infiltration in the pulp tissue. When adenine nucleotides in the pulp tissue of the rat treated with endotoxin was analyzed by HPLC, AMP increased and ATP decreased aignificantly. Histological study revealed that endotoxin caused deformation of nuclei of pulp cells. However, inflammatory responses such as leukocyte infiltration or vasodilatation waer not observed. These results suggest that systemic administration of endotoxin to the rat induces ischemic tissue injury int he dental pulp. In the present study the mechanism of leukocyte-induced platelet adhesion to endothelial cells in vitro was also investigated. It was shown that the platelet adhesion was accompanied by a decrease in platelet cGMP platelet cGMP but not cAMP production is partially involved in the mechanism of leulocyte-induced platelet adhesion.