Differences in control of parasympathetic vasodilation between submandibular and sublingual glands in the rat
Differences in control of parasympathetic vasodilation between submandibular and sublingual glands in the rat
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DOI：
10.1152/ajpregu.00306.2015
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发表时间：
2015-12-01
影响因子：
2.8
通讯作者：
Ishii, Hisayoshi
中科院分区：
文献类型：
--
作者：
Sato, Toshiya;Ishii, Hisayoshi
用激光散斑成像流量计检测了氨基甲酸乙酯麻醉大鼠舌神经中央切端电刺激时下颌下腺（SMGBF）和舌下腺（SLGBF）的血流变化。LN刺激引起强度和频率相关的SMGBF和SLGBF增加，且SMGBF的增加幅度高于SLGBF的增加幅度。静脉注射自主胆碱能神经节阻滞剂六甲溴铵可显著抑制这两个腺体的增加。抗毒蕈碱剂阿托品明显抑制SMGBF的升高，部分抑制SLGBF的升高。输注血管活性肠肽（VIP）受体拮抗剂可显著抑制阿托品耐药的SLGBF升高，尽管单独使用VIP受体拮抗剂没有影响。LN刺激后恢复到基础血流量水平的时间比给予VIP后短。然而，以剂量依赖的方式给药阿托品后，LN刺激后的恢复时间明显延迟至与给药VIP相同的水平。结果表明：1)LN刺激可引起主要由胆碱能纤维引起的副交感神经SMGBF增加和由胆碱能纤维和非胆碱能纤维引起的副交感神经SLGBF增加；2)vip能机制参与非胆碱能SLGBF增加，并在毒蕈碱机制失活时激活。
We examined blood flow in the submandibular gland (SMGBF) and sublingual gland (SLGBF) during electrical stimulation of the central cut end of the lingual nerve (LN) in the urethane-anesthetized rats using a laser speckle imaging flow meter. LN stimulation elicited intensity- and frequency-dependent SMGBF and SLGBF increases, and the magnitude of the SMGBF increase was higher than that of the SLGBF increase. The increase in both glands was significantly inhibited by intravenous administration of the autonomic cholinergic ganglion blocker hexamethonium. The antimuscarinic agent atropine markedly inhibited the SMGBF increase and partly inhibited the SLGBF increase. The atropine-resistant SLGBF increase was significantly inhibited by infusion of vasoactive intestinal peptide (VIP) receptor antagonist, although administration of VIP receptor antagonist alone had no effect. The recovery time to the basal blood flow level was shorter after LN stimulation than after administration of VIP. However, the recovery time after LN stimulation was significantly delayed by administration of atropine in a dose-dependent manner to the same level as after administration of VIP. Our results indicate that 1) LN stimulation elicits both a parasympathetic SMGBF increase mainly evoked by cholinergic fibers and a parasympathetic SLGBF increase evoked by cholinergic and noncholinergic fibers, and 2) VIP-ergic mechanisms are involved in the noncholinergic SLGBF increase and are activated when muscarinic mechanisms are deactivated.