Kim S, Liu M, Simchon S, Dörscher-Kim J E
Department of Endodontics, School of Dental Medicine University of Pennsylvania, Philadelphia.
Proc Finn Dent Soc. 1992;88 Suppl 1:387-92.
One of the major events involving inflammatory processes is the alteration of microcirculatory hemodynamics by inflammatory mediators released from tissue components. Using modern macrocirculatory techniques, 15 mu radioisotope labeled microspheres, 133Xe washout, laser Doppler flowmetry and double isotopes, 125 and 131I-albumin, and microcirculatory methods, intravital fluorescence microscopy with FITC labeled dextran, we have examined the effects of selected mediators, e.g. 5-hydroxytryptamine (5-HT), prostaglandin E2 (PG-E2), bradykinin (BK), substance P (SP), calcitonin gene related peptide (CGRP) and histamine on blood flow and vascular permeability in the pulp of experimental animals. Surprisingly, SP and CGRP caused weak albumin leakage in the pulp, while the opposite is true in high compliance tissues, such as muscles, suggesting that the vessels in a low compliance environment, such as the pulp, may not be as permeable in response to selected mediators. Intraarterial injection of 5-HT caused a strong vasoconstriction which was mediated by 5-HT1p receptor subtype. The pulpal 5-HT receptor subtype was identified by immunocytochemistry, receptor autoradiography and functional investigations. Intravital fluorescence microscopy observations of the rat incisor preparation showed that histamine, BK and PGE2 increased permeability, whereas isoproteranol caused partial inhibition of the BK-induced increase. In an induced pulpal inflammation model using plaque extract, blood flow increased over 40% in the moderately inflamed pulp, which demonstrated severe vasodilation and polymorpholeukocyte accumulation. In the partially necrotic pulp, blood flow decreased nearly 35%. Results of this study clearly show that there is a high structural/functional correlation in pulpal microcirculation in inflammation. As demonstrated in this presentation, the effects of inflammatory mediators on pulpal microcirculatory hemodynamics are complex.(ABSTRACT TRUNCATED AT 250 WORDS)
涉及炎症过程的主要事件之一是组织成分释放的炎症介质改变微循环血流动力学。我们使用现代大循环技术，如15微米放射性同位素标记微球、133氙洗脱、激光多普勒血流仪和双同位素（125和131I标记白蛋白），以及微循环方法，如用异硫氰酸荧光素标记葡聚糖的活体荧光显微镜，研究了所选介质，如5-羟色胺（5-HT）、前列腺素E2（PG-E2）、缓激肽（BK）、P物质（SP）、降钙素基因相关肽（CGRP）和组胺对实验动物牙髓血流和血管通透性的影响。令人惊讶的是，SP和CGRP在牙髓中引起微弱的白蛋白渗漏，而在高顺应性组织如肌肉中则相反，这表明在低顺应性环境如牙髓中的血管对所选介质的反应可能不那么通透。动脉内注射5-HT会引起强烈的血管收缩，这是由5-HT1p受体亚型介导的。通过免疫细胞化学、受体放射自显影和功能研究确定了牙髓5-HT受体亚型。对大鼠切牙制剂的活体荧光显微镜观察表明，组胺、BK和PGE2增加通透性，而异丙肾上腺素部分抑制BK诱导的增加。在使用菌斑提取物诱导的牙髓炎症模型中，中度炎症牙髓中的血流增加超过40%，表现出严重的血管扩张和多形核白细胞聚集。在部分坏死的牙髓中，血流减少近35%。本研究结果清楚地表明，炎症牙髓微循环中存在高度的结构/功能相关性。如本报告所示，炎症介质对牙髓微循环血流动力学的影响是复杂的。（摘要截断于250字）
