Stern L E, Erwin C R, O'Brien D P, Huang F, Warner B W
Division of Pediatric Surgery, Children's Hospital Medical Center, Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229-3039, USA.
Microsc Res Tech. 2000 Oct 15;51(2):138-48. doi: 10.1002/1097-0029(20001015)51:2<138::AID-JEMT5>3.0.CO;2-T.
The loss of small intestinal mucosal surface area is a relatively common clinical situation seen in both the pediatric and adult population. The most frequent causes include mesenteric ischemia, trauma, inflammatory bowel disease, necrotizing enterocolitis, and volvulus. Following surgical resection, the remnant intestine compensates or adapts to the loss of native bowel by increasing its absorptive surface area and functional capacity. Unfortunately, many patients fail to adapt adequately, and are relegated to lifelong intravenous nutrition. Research into intestinal adaptation following small bowel resection (SBR) has evolved only recently from the gross and microscopic level to the biochemical and genetic level. As understanding of this process has increased, numerous therapeutic strategies to augment adaptation have been proposed. Epidermal growth factor (EGF) is an endogenous peptide that is secreted into the gastrointestinal tract and able to influence gut ontogeny, as well as mucosal healing. Early studies have demonstrated its ability to augment the adaptive process. Focusing on a murine model of massive intestinal loss, the morphological, structural, biochemical, and genetic changes that occur during the intestinal adaptive process will be reviewed. The role of EGF and its receptor as critical mediators of the adaptive process will be discussed. Additionally, the ability of EGF to augment intestinal proliferation and diminish programmed cell death (apoptosis) following SBR will be examined. Enhancing adaptation in a controlled manner may allow patients to transition off parenteral nutrition to enteral feeding and, thereby, normalize their lifestyle.
小肠黏膜表面积的丧失是儿科和成人中较为常见的临床情况。最常见的病因包括肠系膜缺血、创伤、炎症性肠病、坏死性小肠结肠炎和肠扭转。手术切除后，残余肠道通过增加其吸收表面积和功能能力来代偿或适应天然肠段的丧失。不幸的是，许多患者未能充分适应，只能依赖终身静脉营养。小肠切除术后肠道适应的研究直到最近才从大体和微观层面发展到生化和基因层面。随着对这一过程认识的增加，人们提出了许多增强适应的治疗策略。表皮生长因子（EGF）是一种内源性肽，分泌到胃肠道中，能够影响肠道发育以及黏膜愈合。早期研究已证明其增强适应过程的能力。本文将聚焦于大量肠道丧失的小鼠模型，回顾肠道适应过程中发生的形态、结构、生化和基因变化。将讨论EGF及其受体作为适应过程关键介质的作用。此外，还将研究EGF增强小肠切除术后肠道增殖和减少程序性细胞死亡（凋亡）的能力。以可控方式增强适应能力可能使患者从肠外营养过渡到肠内喂养，从而使生活方式正常化。
