选择性炎症介质对牙髓血流和血管通透性的影响。

S Kim, M Liu, S Simchon, J E Dörscher-Kim
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引用次数: 0

摘要

炎症过程的主要事件之一是由组织成分释放的炎症介质改变微循环血流动力学。利用现代大循环技术,15 μ放射性同位素标记微球,133Xe冲洗,激光多普勒血流法和双同位素,125和131i白蛋白,微循环方法,FITC标记葡聚糖的活体荧光显微镜,我们研究了所选介质的影响,如5-羟色胺(5-HT),前列腺素E2 (PG-E2),慢激肽(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在牙髓中引起了微弱的白蛋白渗漏,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)中的血管对特定介质的反应可能不具有渗透性。动脉注射5-羟色胺引起强烈的血管收缩,这种收缩是由5-羟色胺受体亚型介导的。通过免疫细胞化学、受体放射自显影和功能检查确定牙髓5-HT受体亚型。活体荧光显微镜观察显示,组胺、BK和PGE2增加了切牙的通透性,而异丙醇部分抑制了BK诱导的通透性增加。在使用斑块提取物诱导的牙髓炎症模型中,中度炎症牙髓的血流量增加了40%以上,这表明严重的血管扩张和多形白细胞积聚。在部分坏死的牙髓中,血流量减少了近35%。本研究结果清楚地表明,牙髓微循环在炎症中具有高度的结构/功能相关性。正如本报告所展示的,炎症介质对牙髓微循环血流动力学的影响是复杂的。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of selected inflammatory mediators on blood flow and vascular permeability in the dental pulp.

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)

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