Hölzer H H, Turkelson C M, Solomon T E, Raybould H E
Veterans Affairs/University of California Los Angeles Gastroenteric Biology Center.
Am J Physiol. 1994 Oct;267(4 Pt 1):G625-9. doi: 10.1152/ajpgi.1994.267.4.G625.
The mechanism by which lipid in the duodenum inhibits gastric emptying was investigated in awake rats fitted with chronic gastric and duodenal cannulas. Perfusion of the duodenum with lipid (Intralipid, 5 and 10%; total amount 50 and 100 mg) caused a significant inhibition (26 and 78%, respectively) of gastric emptying of a nonnutrient liquid (0.9% saline). Functional ablation of the capsaicin-sensitive vagal, but not the spinal, sensory innervation to the upper gastrointestinal tract significantly attenuated by 57% lipid-induced inhibition of gastric emptying. In intact rats, administration of a specific cholecystokinin (CCK)-A receptor antagonist, devazepide, significantly attenuated by 66% the response to lipid. Administration of devazepide in perivagal capsaicin-treated rats did not further reduce the response to lipid. These results suggest that lipid in the duodenum inhibits gastric emptying via a mechanism involving an action of CCK at type A receptors and capsaicin-sensitive vagal afferents.
在装有慢性胃和十二指肠插管的清醒大鼠中,研究了十二指肠内脂质抑制胃排空的机制。用脂质(英脱利匹特,5%和10%;总量50和100毫克)灌注十二指肠,可显著抑制(分别为26%和78%)非营养性液体(0.9%盐水)的胃排空。对上消化道的辣椒素敏感迷走神经而非脊髓感觉神经支配进行功能性切除,可使脂质诱导的胃排空抑制显著减轻57%。在完整大鼠中,给予特异性胆囊收缩素(CCK)-A受体拮抗剂地伐西匹,可使对脂质的反应显著减轻66%。在经迷走神经周围辣椒素处理的大鼠中给予地伐西匹,并未进一步降低对脂质的反应。这些结果表明,十二指肠内的脂质通过一种涉及CCK对A型受体的作用和辣椒素敏感迷走神经传入纤维的机制来抑制胃排空。