Barreto Savio G, Windsor John A
Hepatobiliary and Oesophagogastric Unit, Division of Surgery and Perioperative Medicine, Flinders Medical Centre, Bedford Park, Adelaide, SA, Australia.
HBP/Upper GI Unit, Department of General Surgery, Auckland City Hospital, Auckland, New Zealand.
Dig Dis Sci. 2017 Feb;62(2):319-335. doi: 10.1007/s10620-016-4402-0. Epub 2016 Dec 19.
Delayed gastric emptying (DGE) represents a significant cause for morbidity following pancreatoduodenectomy (PD). At a time when no specific and universally effective therapy exists to treat these patients, elucidating other potential (preventable or treatable) mechanisms for DGE is important. The aim of the manuscript was to test the hypothesis that ileal brake contributes to DGE in PD patients receiving jejunal tube feeding by systematically reviewing experimental and clinical literature. A series of clinically relevant questions were framed related to the potential role of the ileal brake in development of DGE post-PD and formed the basis of targeted literature searches. A comprehensive search of major reference databases from January 1980 to June 2015 was carried out which included human and animal studies. The ileal brake is a feedback loop neurally mediated by the vagus and sympatho-adrenergic pathways and hormonally by gut peptides including glucagon-like peptide-1, peptide YY (PYY), and neurotensin. The most potent stimulus for this inhibitory reflex is intra-ileal fat. There is evidence to indicate the role of an inhibitory reflex (on gastric emptying) mediated by PYY and CCK which, in turn, are stimulated by nutrient delivery into the distal small intestine providing indirect support to the role of ileal brake in post-PD DGE. The ileal brake is a likely factor contributing to DGE post-PD. While there has been no study to directly test this hypothesis, there is compelling indirect evidence to support it. Designing a trial that would answer such a question appears to be the most appropriate way forward.
胃排空延迟（DGE）是胰十二指肠切除术（PD）后发病的一个重要原因。在尚无特异性且普遍有效的治疗方法来治疗这些患者的情况下，阐明DGE的其他潜在（可预防或可治疗）机制非常重要。本文的目的是通过系统回顾实验和临床文献，检验回肠制动在接受空肠管饲的PD患者发生DGE中起作用这一假说。针对回肠制动在PD术后DGE发生中的潜在作用，提出了一系列与临床相关的问题，并构成了针对性文献检索的基础。对1980年1月至2015年6月的主要参考文献数据库进行了全面检索，包括人类和动物研究。回肠制动是一种由迷走神经和交感 - 肾上腺素能途径神经介导、由包括胰高血糖素样肽 -1、肽YY（PYY）和神经降压素在内的肠道肽激素介导的反馈回路。这种抑制性反射最有力的刺激因素是回肠内脂肪。有证据表明由PYY和胆囊收缩素介导的（对胃排空的）抑制性反射的作用，而PYY和胆囊收缩素又受到营养物质进入远端小肠的刺激，这为回肠制动在PD术后DGE中的作用提供了间接支持。回肠制动可能是导致PD术后DGE的一个因素。虽然尚无研究直接验证这一假说，但有令人信服的间接证据支持它。设计一项能够回答此类问题的试验似乎是最恰当的前进方向。
