Mesquita M A, Thompson D G, Troncon L E, D'Amato M, Rovati L C, Barlow J
Department of Medicine, Hope Hospital, University of Manchester School of Medicine, Salford, United Kingdom.
Am J Physiol. 1997 Jul;273(1 Pt 1):G118-23. doi: 10.1152/ajpgi.1997.273.1.G118.
The purpose of this study was to assess the role of endogenous cholecystokinin (CCK) in regulating fat-induced changes in human gastric relaxation. Proximal gastric pressure-volume relationships were determined in 12 healthy volunteers during a series of gastric distensions, both fasting and after intragastric instillation of 250 ml of 10% Intralipid. All subjects were studied twice, in a randomized, double-blind study, during intravenous infusion of either loxiglumide (CCK-A antagonist) or saline. For each distension, intragastric pressure and compliance were determined together with perception intensity. During saline infusion, Intralipid reduced intragastric pressure (prelipid, 11.7 +/- 0.8; postlipid, 9.7 +/- 0.6 mmHg; P = 0.002) and increased compliance (pressure-volume slope values: prelipid, 87.6 +/- 9.7; postlipid, 47.2 +/- 7; P < 0.01). Loxiglumide infusion during fasting exerted no effect on either intragastric pressure or compliance. After lipid, however, loxiglumide abolished the expected postlipid reduction in intragastric pressure (prelipid, 12.1 +/- 0.7; postlipid, 11.5 +/- 0.8 mmHg; P = 0.4) but did not consistently abolish the postlipid increase in compliance. Loxiglumide exerted no effect on the cumulative perception score or on the volume at perception threshold, although it prevented the fat-induced reduction in pressure at perception threshold [control: prelipid, 15.4 +/- 1.1; postlipid, 10.7 +/- 0.5 (P < 0.05); loxiglumide: prelipid, 13.8 +/- 1.5; postlipid, 12.2 +/- 0.9 (P > 0.05)]. Endogenous CCK or CCK-A receptors therefore play a role in the fat-induced reduction of intragastric pressure and might also modulate gastric perception after lipid.
本研究旨在评估内源性胆囊收缩素（CCK）在调节脂肪引起的人体胃舒张变化中的作用。在一系列胃扩张过程中，对12名健康志愿者进行了近端胃压力-容积关系测定，测定时分别处于空腹状态以及胃内注入250 ml 10%英脱利匹特之后。在静脉输注洛西格列肽（CCK-A拮抗剂）或生理盐水的随机双盲研究中，所有受试者均接受了两次研究。对于每次扩张，均测定胃内压力和顺应性以及感知强度。在输注生理盐水期间，英脱利匹特降低了胃内压力（输注脂质前，11.7±0.8；输注脂质后，9.7±0.6 mmHg；P = 0.002）并增加了顺应性（压力-容积斜率值：输注脂质前，87.6±9.7；输注脂质后，47.2±7；P < 0.01）。空腹期间输注洛西格列肽对胃内压力或顺应性均无影响。然而，在输注脂质后，洛西格列肽消除了预期的输注脂质后胃内压力降低（输注脂质前，12.1±0.7；输注脂质后，11.5±0.8 mmHg；P = 0.4），但并未始终消除输注脂质后顺应性的增加。洛西格列肽对累积感知评分或感知阈值时的容积均无影响，尽管它阻止了脂肪引起的感知阈值时压力降低[对照组：输注脂质前，15.4±1.1；输注脂质后，10.7±0.5（P < 0.05）；洛西格列肽组：输注脂质前，13.8±1.5；输注脂质后，12.2±0.9（P > 0.05）]。因此，内源性CCK或CCK-A受体在脂肪引起的胃内压力降低中起作用，并且可能也调节脂质后的胃感知。
