Monitoring of oxygen-derived radicals : development and appplication of optical biosensor to oral tissues under pathological conditions

反应性充血，局部血管扩张，由于氧气不足和由于血流中断而积聚的代谢废物；活动性充血，以及在活动期间器官内血流量的增加。微循环部分由交感神经控制，部分由内皮细胞局部分泌的血管活性物质控制。后者中最重要的是一氧化氮(NO)，它通过使血管平滑肌松弛来促进血流。本研究采用激光多普勒血流仪和NO电化学技术，研究了NO在反应性充血时牙龈局部循环调节中的作用。用激光多普勒血流仪测量右下颌尖牙附着牙周组织中的牙周血流量。反应性充血可诱发…通过释放闭合压力(30、60和300s)，激光多普勒血流计探头以小于2ml/min/100g的压力作用于牙龈组织。为了对牙龈组织产生的反应性充血进行药理学研究，给出了各种药物的动脉内团注。结果：通过对牙龈组织进行闭塞30、60和300s的压迫，牙周血流量随着闭塞时间的增加而增加。预先给予一氧化氮合酶抑制剂N-ω-硝基-L-精氨酸甲酯(N-NAME，60 mg/kg，i.a.)可明显抑制反应性充血，但不能被M受体拮抗剂阿托品、β阻滞剂心得安、H1阻断剂毛胺、H2阻断剂西咪替丁所抑制。静脉注射一氧化氮合酶底物L精氨酸(60 mg/kg)可部分恢复L抑制的牙龈反应性充血。结论：NO作为非肾上腺素能非胆碱能(NANC)介质参与了牙龈组织反应性充血时的血管扩张，参与了牙周循环内环境平衡的维持。较少

Reactive hyperemia, the local vasodilatation which occurs in response to oxygen debt and accumulation of metabolic waste products due to interruption of blood flow ; active hyperemia, and the increased blood flow in an organ during a period of activity. The microcirculation is controlled partly by sympathetic nerve and partly by vasoactive substances secreted locally by the endothelial cells. The most important of the latter is nitric oxide(NO), which facilitates flow by causing relaxation of vascular smooth muscle. In the present study, we investigated the role of NO in the regulation of local circulation in gingival tissue during reactive hyperemia, using laser Doppler flowmetry and NO electrochemical technique.METHODS : The experiments were performed in beagle dogs under anesthesia by sodium pentobarbital (25 mg/kg, i.v.). Gingival blood flow (GBF) was measured in attached gingival tissue of right mandibular canine tooth using a laser Doppler flowmeter. Reactive hyperemia was elicit … More ed by release of occlusive compression (30, 60 and 300 sec period), which laser Doppler flowmeter probe was applied against to the gingival tissue at a force that caused less than GBF 2 ml/min/100 g. In order to perform pharmacological consideration of reactive hyperemia generated in gingival tissue, intra-arterial bolus injection of various drugs were given.RESULTS : The GBF increased depending on occlusion durations of 30, 60, and 300 sec by compressing of gingival tissue. The reactive hyperemia was significantly suppressed by pretreatment with N ω-nitro-L-arginine methyl ester (L-NAME, 60 mg/kg, i.a.), an inhibitor of NO synthase, but not by atropine (muscarinic antagonist), propranolol(β-blocker), pilylamine (H1-blocker), cimetidine (H2-blocker). The L-NAME-suppressed reactive hyperemia in gingiva was partially recovered by the treatment with L-arginine (60 mg/kg, i.a.), the substrate of NO synthase. Furthermore, NO could be detected using NO-selective electrode during reactive hyperemia in gingival tissue.CONCLUSIONS : These results suggest that NO function as nonadrenergic noncholinergic (NANC) mediator is involved in the vasodilation during reactive hyperemia in gingival tissue, and deals with the maintenance of homeostasis in gingival circulation. Less