精氨酸促进短肠综合征肠道代偿及其机制的初步研究

Effect of enteral supplement of arginine on intestinal adaptation and its mechanism in experimental rats with short bowel syndrome

目的研究肠内营养中添加精氨酸对广泛肠切除术后大鼠肠道代偿的影响。方法将30只SD大鼠随机分为Con组（假手术）、SB组（短肠对照）和SB—Arg组（短肠加用精氨酸），各组大鼠于术后第2。14天分别给予等氮、等热量的肠内营养支持．其中SB-Arg组肠内营养中添加L-精氨酸（300mg·kg^-1·d^-1）。比较术后各组体质量、脂肪吸收率、血浆总游离脂肪酸及必需脂肪酸水平、小肠代偿指标、肠黏膜细胞增殖和凋亡的差异。结果SB组术后早期营养支持2周后，其体质量较Con组低，各项肠道代偿指标均明显升高（P〈0．05）。SB-Arg组大鼠脂肪吸收率[（84．9±3．2）％]、血浆游离脂肪酸水平[（650．0±86．5）mg／L]、回肠黏膜质量[（18．0±3．5）mg·cm^-1·100g^-1]、回肠DNA含量[（29．6±3．3）μg·cm^-1·100g^-1]、小肠蛋白质含量[空肠（65．5＋7．3）μg·cm^-1·100g^-1和回肠（39．2±2．3）μg·cm^-1·100g^-1]和小肠增殖指数（空肠31±4，回肠32±2）均高于SB组的[（81．3±3．9）％、（289．5±76．9）mg／L、（13．5±3．0）mg·cm^-1·100g^-1（26．0＋2．6）μg·cm^-1·100g^-1（59．8±6．2）μg·cm^-1·100g^-1、（35．4±2．3）μg·cm^-1·100g^-1、（22±3）及（25±3），均P〈0．05]；小肠超微结构亦观察到SB-Arg组大鼠小肠绒毛高度、隐窝深度及黏膜厚度均大于SB组大鼠（P〈0．05）。结论肠内营养中添加适量精氨酸能促进短肠综合征大鼠肠道结构及功能的代偿．其机制可能为促进肠黏膜细胞增殖、抑制其凋亡。

Objective To evaluate the effect of enteral supplement of arginine on intestinal adaptation in rats with short bowel syndrome（SBS） and to study its mechanism. Methods SD rats were randomly assigned to three groups： sham rats （Con）, SBS rats （SB） and SBS rats supplemented with enteral arginine （SB-Arg）. All the animals received isonitrogenic and isocaloric enteral nutrition, except that SB-Arg rats received enteral nutrition supplemented with arginine （300 mg·kg·d^-1）. Fat absorbability, plasma free fatty acids, parameters of intestinal adaptation, enterocytes proliferation and apoptosis were determined. Results After massive small bowel resection, rats had significant bowel adaptation. Compared with SB rats, SB-Arg rats demonstrated a significant increase in fat absorbability [ （84.9±3.2）% vs [ （81.3±3.9）%], plasma level of free fatty acids[ （650.0±86.5） vs （289.5±76.9） mg/L], ileal mucosal weight [ （18.0±3.5） vs （13.5±3.0） mg·cm^-1·100g^-1], ileal DNA content [ （29.6±3.3） vs （26.0±2.6）μg·cm^-1·100g^-1], jejunal mucosal protein content [ （65.5±7.3） vs （59.8±6.2） μg·cm^-1·100g^-1, ileal mueosal protein content [ （39.2±2.3） vs （35.4±2.3） μg·cm^-1·100g^-1], jejunal mucosal proliferation index [31±4 vs 22±3] and ileal mucosal proliferation index [32±2 vs 25±3] （all P〈0.05）. Moreover, jejunal and ileal villus length, crypt depth and mucosal thickness in SBS-Arg rats were higher than those in SB rats （P〈0.05）. Conclusions In rat SBS model, enteral supplement of arginine appears to stimulate intestinal structural and functional adaptation. The mechanism may be that arginine can stimulate enterocyte proliferation and inhibit enterocyte apoptosis.