[用激光多普勒测量猫的牙龈血管逆行扩张]。

S Kuriwada
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引用次数: 1

摘要

本研究旨在探讨电刺激猫下牙槽神经(IAN)引起牙龈血管扩张的机制。用戊巴比妥钠(30mg /kg,静脉注射)麻醉55只幼猫(2-4 kg)。手术暴露后,采用激光多普勒测速仪(LDV)无创技术连续测量龈血流量(GBF)。实验过程中监测体表血压。电刺激切开的IAN远端导致GBF增加,但胍乙啶治疗猫的血压没有改变。刺激强度(20 ~ 80 V)和刺激持续时间(0.2 ~ 5秒)均影响刺激强度的增加。在两次刺激之间休息10分钟,观察到的GBF增加在100分钟内是可重复的。静脉注射(D-Pro2, d - try7,9)- P物质、三倍南胺和甲基塞吉内酯后,电刺激IAN引起的GBF增加分别被66.8 +/- 7.3%、51.1 +/- 3%、37.8 +/- 4.6%(平均+/- S.E.M.)显著抑制。另一方面,静脉注射阿托品、心得安、六甲溴铵或西咪替丁对电刺激IAN引起的GBF升高无影响。这些结果表明,电刺激后猫的牙龈血管扩张是由感觉神经释放P物质引起的,而P物质的释放又刺激肥大细胞释放组胺或血清素,从而引起血管扩张。
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[Antidromic vasodilatation in the cat gingiva as measured by laser Doppler].

The present study was designed to investigate the mechanism of gingival vasodilatation induced by electrical stimulation of the inferior alveolar nerve (IAN) in cats. A total of 55 young cats (2-4 kg) were anesthetized with pentobarbital sodium (30 mg/kg, i.v.). After IAN was surgically exposed, gingival blood flow (GBF) was continuously measured with the noninvasive technique of using a laser Doppler velocimeter (LDV). The systemic blood pressure was monitored during the experiment. Electrical stimulation of the distal end of the cut IAN led to a GBF increase with no alteration of the blood pressure in guanethidine treated cats. These increases were dependent on both the stimulus intensity (20-80 V) and the stimulus duration (0.2-5 sec). The GBF increases observed were reproducible for 100 min, when a resting period of 10 min was allowed between stimulations. The GBF increase by electrical stimulation of IAN was significantly inhibited by 66.8 +/- 7.3%, 51.1 +/- 3%, 37.8 +/- 4.6% (mean +/- S.E.M.) after i.v. injection of (D-Pro2, D-Try7,9)-substance P, triplennamine or methysergide, respectively. I.v. injection of atropine, propranolol, hexamethonium or cimetidine, on the other hand, had no effect on the GBF increase by electrical stimulation of IAN. These results suggest that gingival vasodilatation following electrical stimulation of IAN in cats is initiated by the peripheral release of substance P from sensory nerves, and that the substance P released, in turn, stimulates the mast cells to release histamine or serotonin which causes the vasodilatation.

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