Somatic electrical nerve stimulation regulates the motility of sphincter of Oddi in rabbits and cats - Evidence for a somatovisceral reflex mediated by cholecystokinin
Somatic electrical nerve stimulation regulates the motility of sphincter of Oddi in rabbits and cats - Evidence for a somatovisceral reflex mediated by cholecystokinin
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DOI：
10.1023/a:1018870017774
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发表时间：
1999-09-01
影响因子：
3.1
通讯作者：
Hong, CY
中科院分区：
文献类型：
--
作者：
Chiu, JH;Kuo, YL;Hong, CY
CCK在草食和肉食动物的胆汁运动中起着重要的调节作用。关于Oddi括约肌(SO)的运动是如何通过躯体刺激来调节的，人们知之甚少。我们的目的是验证躯体神经电刺激(SENS)通过CCK相关机制影响不同类型SO动物SO运动的假说。用持续灌流开放顶端测压的方法测定麻醉兔和猫的SO活性。在右侧锁骨中线第6和第7肋间间隙靠近脊神经的两根针上交替施加电流(2/15赫兹，20min)，产生SENS。记录SENS开始前和开始后X分钟的SO运动，分别记为PREEP-SENS和SENS-X，并保存在装有离线分析软件的计算机中。与SENS前相比，SENS期间兔的SO活性显著升高，其收缩时相压力和总和峰值持续时间均显著高于SENS前。Pre-SENS、SENS-10和SENS-16的时相收缩压分别为6.83±0.39 mm Hg、9.23±0.83 mm Hg和10.46±0.81 mm Hg(P<；0.03，N=13)。Pre-SENS、SENS-10和SENS-16的求和峰值持续时间分别为7.26±0.41秒、10.22±0.46秒和13.49±2.31秒(P<；0.05，N=13)。预先给予阿托品、心得安、酚妥拉明或纳洛酮不能抑制SENS诱导的SO过度活动，但可被CCK受体拮抗剂丙谷胺和抗CCK-8抗体以剂量依赖的方式阻断。相反，SENS在猫身上诱导了一种抑制性的SO反应。然而，在两种情况下，放射免疫法测定的血浆CCK水平在SENS后均明显升高。我们的结论是，SENS导致CCK的分泌，进而影响不同类型SO动物的胆道运动。这为SO功能亢进的患者提供了一种简单实用的方法。
Cholecystokinin (CCK) plays an important role in regulating the biliary motility in herbivorous and carnivorous animals. Little is known about how the motility of the sphincter of Oddi (SO) is regulated through a somatic stimulation. It was our aim to test the hypothesis that somatic electrical nerve stimulation (SENS) affects SO motility in animals with different types of SO through CCK-related mechanisms. The activity of SO in anesthetized rabbits and cats was measured by using a continuously perfused open-tip manometric method. SENS was brought about by applying an electric current (2/15 Hz alternatively, 20 min) to two needles positioned near spinal nerves in the 6th and 7th intercostal space in the right midclavicular line. The SO motility before and X min after the start of SENS, designated as pre-SENS and SENS-X respectively, were recorded and saved in a computer equipped with off-line analysis software. The SO activity in rabbits, in terms of phasic contraction pressure and duration of summation peak during SENS were significantly higher than that before SENS. The phasic contraction pressure of pre-SENS, SENS-10, and SENS-16 were 6.83 +/- 0.39 mm Hg, 9.23 +/- 0.83 mm Hg and 10.46 +/- 0.81 mm Hg, respectively (P < 0.03, N = 13). The duration of summation peak in pre-SENS, SENS-10, and SENS-16 were 7.26 +/- 0.41 sec, 10.22 +/- 0.46 sec, and 13.49 +/- 2.31 sec, respectively (P < 0.05, N = 13). The SENS-induced SO hyperactivity was not inhibited by pretreatment with atropine, propranolol, phentolamine, or naloxone, but was blocked by pretreatment with the CCK receptor antagonist, proglumide, and by injection of anti-CCK-8 antibody during SENS in a dose-dependent manner. In contrast, SENS induced an inhibitory SO response in cats. However, in both circumstances, an obvious elevation of plasma CCK level determined by radioimmunoassay was noted after SENS. We conclude that SENS causes secretion of CCK, which in turn affects biliary tract motility in animals with different types of SO. This provides an easily applicable method for those patients who have hyperactive SO function.