Olsson C, Aldman G, Larsson A, Holmgren S
Department of Zoophysiology, University of Göteborg, Box 463, S-405 30 Göteborg, Sweden and Department of Radiation Physics, Sahlgrenska Hospital, Göteborg, Sweden.
J Exp Biol. 1999 Jan;202(Pt 2):161-70. doi: 10.1242/jeb.202.2.161.
In this study, we describe new methods for recording gastric emptying and in vivo measurements of intragastric pressure in fish. Using these methods, we investigated the effects of the sulphated octapeptide of cholecystokinin (CCK8) on gastric emptying and on stomach motility in vivo and in vitro. Gastric emptying of 99Tcm-labelled food was measured in swimming fish by using a gamma camera, counting consecutive 2.5 min periods for 18-42 h. After 20 h, 55.3+/-4.0 % of the labelled food remained in the stomach of the control fish (mean s.e.m., N=9). Vascular infusion of CCK8 (25 pmol kg-1 h-1) delayed gastric emptying so that 70.4+/-4.8 % of the labelled food remained in the stomach after 20 h (N=8). Gastric pressure changes in vivo were measured using a balloon surgically fitted into the cardiac or pyloric part of the stomach. In the cardiac part, intra-arterial infusion of CCK8 at 0.1 nmol kg-1 h-1 resulted in a decrease in the frequency and amplitude of rhythmic contractions, while higher doses started/increased contractions. Atropine blocked much of the basal contractile activity, but did not influence the CCK8-induced inhibition of contractile activity. The pyloric part of the stomach was unaffected by intra-arterial infusion of CCK8 or atropine. In vitro perfusion of the stomach (with a balloon placed in the cardiac part to record motility) with CCK8 at high concentrations (10(-7 )mol l-1 and above) augmented the spontaneous contractions, while lower concentrations had inconsistent effects. In addition, CCK8 (10(-7) to 10(-6 )mol l-1) decreased the amplitude of spontaneous contractions in longitudinal strip preparations, usually in combination with an increase in the resting tension. The decrease in amplitude was not affected by the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester hydrochloride (L-NAME; 10(-4 )mol l-1). Depending on the concentration and experimental arrangement, CCK8 had either inhibitory or excitatory effects on the cardiac stomach, suggesting the possible presence of different types of CCK receptor. We conclude that the predominant effect of CCK8 in vivo may be a slowing down of gastric emptying, presumably coinciding with a release of bile into the duodenum.
在本研究中，我们描述了记录鱼类胃排空及胃内压活体测量的新方法。利用这些方法，我们研究了胆囊收缩素的硫酸化八肽（CCK8）对体内和体外胃排空及胃动力的影响。通过使用γ相机，对游动的鱼体内99锝标记食物的胃排空进行测量，连续计数2.5分钟时间段，持续18 - 42小时。20小时后，对照鱼胃内仍有55.3±4.0%的标记食物（平均值±标准误，N = 9）。血管内输注CCK8（25 pmol kg-1 h-1）延迟了胃排空，使得20小时后胃内仍有70.4±4.8%的标记食物（N = 8）。使用手术植入胃贲门或幽门部的气球测量体内胃压力变化。在贲门部，以0.1 nmol kg-1 h-1的剂量动脉内输注CCK8导致节律性收缩的频率和幅度降低，而更高剂量则引发/增强收缩。阿托品阻断了大部分基础收缩活动，但不影响CCK8诱导的收缩活动抑制。胃幽门部不受动脉内输注CCK8或阿托品的影响。用高浓度（10(-7) mol l-1及以上）的CCK8对胃进行体外灌注（在贲门部放置气球记录动力）增强了自发收缩，而较低浓度的效果则不一致。此外，CCK8（10(-7)至10(-6) mol l-1）降低了纵向肌条标本中自发收缩的幅度，通常伴随着静息张力的增加。幅度的降低不受一氧化氮合酶抑制剂盐酸NG-硝基-L-精氨酸甲酯（L-NAME；10(-4) mol l-1）的影响。根据浓度和实验设置，CCK8对贲门胃既有抑制作用也有兴奋作用，提示可能存在不同类型的CCK受体。我们得出结论，CCK8在体内的主要作用可能是减缓胃排空，推测这与胆汁排入十二指肠同时发生。
