Adelson David W, Million Mulugeta, Kanamoto Koki, Palanca Tiffany, Taché Yvette
Digestive Diseases Research Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90073, USA.
Am J Physiol Gastrointest Liver Physiol. 2004 Feb;286(2):G321-32. doi: 10.1152/ajpgi.00057.2003.
Gastric and sphincter motility evoked by intravenous injection of CCK-8 were investigated in urethane-anesthetized rats. Digital ultrasonomicrometry was used to monitor pyloric (PYL), antral (ANT), corpus (COR), and lower esophageal sphincter (LES) movements while simultaneously measuring intragastric pressure (IGP) and, in some experiments, subdiaphragmatic intraesophageal pressure (sIEP). Intracrystal distances (ICD) were measured continuously between pairs of piezoelectric crystals affixed to the serosa of PYL, ANT, COR (circular and longitudinal), and LES. Consecutive intravenous injections of CCK-8 (0.3, 1, and 3 microg/kg) at 30-min intervals caused dose-dependent simultaneous tonic contractions of PYL and ANT, LES opening, and drops in IGP with peak changes at 3 microg/kg of -17.9 +/- 2.1, -7.7 +/- 2.5, 6.5 +/- 1.4, and -29.2 +/- 3.8%, respectively, whereas intravenous saline had no effect. Rhythmic contractile activity was inhibited by CCK-8. COR responses were not significantly different from vehicle controls for most metrics, and the direction of response for circular COR varied between preparations, although not for repeated trials in a single preparation. During the LES response to CCK-8, sIEP rose in parallel with drops in IGP, indicating formation of a common cavity. Recovery of LES ICD after intravenous CCK occurred more rapidly than recovery of PYL ICD, suggesting the importance of preventing simultaneous patency of gastroesophageal and gastroduodenal passages. The CCK(A) receptor antagonist devazepide (500 microg/kg intravenous) inhibited motion responses evoked by intravenous CCK-8. These data revealed CCK-8-induced gastric and sphincter activity consistent with retropulsion of gastric content.
在氨基甲酸乙酯麻醉的大鼠中，研究了静脉注射CCK-8诱发的胃和括约肌运动。使用数字超声测微法监测幽门（PYL）、胃窦（ANT）、胃体（COR）和食管下括约肌（LES）的运动，同时测量胃内压（IGP），在一些实验中还测量膈下食管内压（sIEP）。连续测量固定在PYL、ANT、COR（环形和纵形）和LES浆膜上的一对压电晶体之间的晶内距离（ICD）。以30分钟的间隔连续静脉注射CCK-8（0.3、1和3微克/千克），可引起PYL和ANT、LES开放的剂量依赖性同时强直性收缩，以及IGP下降，在3微克/千克时峰值变化分别为-17.9±2.1%、-7.7±2.5%、6.5±1.4%和-29.2±3.8%，而静脉注射生理盐水则无影响。CCK-8抑制节律性收缩活动。对于大多数指标，COR反应与溶剂对照组无显著差异，尽管在单个制剂中重复试验时并非如此，但环形COR的反应方向在不同制剂之间有所不同。在LES对CCK-8的反应过程中，sIEP与IGP下降同时升高，表明形成了一个共同腔。静脉注射CCK后LES的ICD恢复比PYL的ICD恢复更快，这表明防止胃食管和胃十二指肠通道同时开放很重要。CCK（A）受体拮抗剂地伐西匹（500微克/千克静脉注射）抑制静脉注射CCK-8诱发的运动反应。这些数据揭示了CCK-8诱导的胃和括约肌活动与胃内容物的逆行推进一致。
