十二指肠脂质及胆囊收缩素A受体在功能性消化不良病理生理学中的作用
Role of duodenal lipid and cholecystokinin A receptors in the pathophysiology of functional dyspepsia.
作者信息
Feinle C, Meier O, Otto B, D'Amato M, Fried M
机构信息
Gastroenterology Division, University Hospital Zürich, Switzerland.
出版信息
Gut. 2001 Mar;48(3):347-55. doi: 10.1136/gut.48.3.347.
BACKGROUND/AIMS: We aimed to evaluate the role of fat and cholecystokinin (CCK) in the pathophysiology of functional dyspepsia (FD) by investigating symptoms and plasma CCK levels following increasing doses of duodenal lipid during gastric distension, and the effect of CCK-A receptor blockade.
SUBJECTS/METHODS: In study A, six FD patients were studied on three occasions during duodenal infusion of saline or lipid (1.1 (L-1) or 2 kcal/min (L-2)) and proximal gastric distensions. Six healthy subjects were also studied as controls during L-2 only. In study B, the effect of the CCK-A antagonist dexloxiglumide (5 mg/kg/h) on L-2 induced symptoms was studied in 12 FD patients. Changes in gastric volume at minimal distending pressure and plasma CCK (study A) were assessed, gastric distensions were performed using a barostat, and dyspeptic symptoms were monitored.
RESULTS
Lipid increased gastric volume compared with saline (DeltaV (ml): saline 15 (20), L-1 122 (42), L-2 114 (28)) in patients and even more so in controls (221 (37); p<0.05). During distensions, symptoms were greater during L-2 than during saline or L-1, and greater in patients than in controls, while gastric compliance was smaller in patients than in controls (p<0.05). Lipid increased plasma CCK levels in patients and controls (p>0.05). Dexloxiglumide abolished the increase in gastric volume (DeltaV (ml): dexloxiglumide 17 (9), placebo 186 (49)) and dyspeptic symptoms (sum of scores: dexloxiglumide 24 (7), placebo 44 (19)) during duodenal lipid infusion. Dexloxiglumide also reduced gastric compliance (ml/mm Hg: dexloxiglumide 51 (7), placebo 72 (11)) and symptoms (sum of scores: dexloxiglumide 101 (17), placebo 154 (21)) during gastric distension.
CONCLUSION
CCK-A receptors are involved in the generation of dyspeptic symptoms by duodenal lipid during gastric distension.
背景/目的：我们旨在通过研究胃扩张期间十二指肠脂质剂量增加后的症状和血浆胆囊收缩素（CCK）水平，以及CCK - A受体阻断的作用，来评估脂肪和CCK在功能性消化不良（FD）病理生理学中的作用。
受试者/方法：在研究A中，6例FD患者在十二指肠输注生理盐水或脂质（1.1千卡/分钟（L - 1）或2千卡/分钟（L - 2））以及近端胃扩张期间进行了3次研究。6名健康受试者仅在L - 2期间作为对照进行了研究。在研究B中，对12例FD患者研究了CCK - A拮抗剂右旋洛醋胺（5毫克/千克/小时）对L - 2诱导症状的影响。评估了最小扩张压力下胃容积和血浆CCK的变化（研究A），使用气压调节装置进行胃扩张，并监测消化不良症状。
结果
与生理盐水相比，脂质增加了患者的胃容积（ΔV（毫升）：生理盐水15（20），L - 1 122（42），L - 2 114（28）），在对照组中增加得更多（221（37）；p<0.05）。在扩张期间，L - 2期间的症状比生理盐水或L - 1期间更严重，患者比对照组更严重，而患者的胃顺应性比对照组小（p<0.05）。脂质增加了患者和对照组的血浆CCK水平（p>0.05）。右旋洛醋胺消除了十二指肠脂质输注期间胃容积的增加（ΔV（毫升）：右旋洛醋胺17（9），安慰剂186（49））和消化不良症状（评分总和：右旋洛醋胺24（7），安慰剂44（19））。右旋洛醋胺还降低了胃扩张期间的胃顺应性（毫升/毫米汞柱：右旋洛醋胺51（7），安慰剂72（11））和症状（评分总和：右旋洛醋胺101（17），安慰剂154（21））。
结论
CCK - A受体参与胃扩张期间十二指肠脂质引起的消化不良症状的产生。
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