Bhatia A M, Feddersen R M, Musemeche C A
Department of Surgery, University of New Mexico Health Sciences Center, Albuquerque 87131-5341, USA.
J Surg Res. 1996 Jun;63(1):152-6. doi: 10.1006/jsre.1996.0239.
Necrotizing enterocolitis (NEC) develops primarily after the onset of enteral feeds in the premature infant. The purpose of this study was to evaluate the influence of intestinal luminal nutrients on histologic injury and the oxidant response in a rat model of NEC. On postnatal Days 10 and 35, Sprague-Dawley rats (total n = 81) underwent abdominal laparotomy. A control group received sham-injury only. The ischemia groups received a single intraluminal injection of 0.25 ml (Day 10) or 1.0 ml (Day 35) of lactose (8.6 g/dl), casein (2.2 g/dl), corn oil (4.4 g/dl), or infant formula (Similac; 20 g/dl). After injection of the nutrient solutions, ischemia groups underwent mesenteric occlusion for 1 hr and intraluminal injection of platelet-activating factor (50 microgram/kg). Necropsies were performed after 6 hr or at demise. Intestinal samples were taken for histology, total glutathione (GSH; an antioxidant), and conjugated dienes (a lipid peroxidation product). Histologic injury was scored from 0 (normal) to 5 (transmural necrosis). Microscopic injury scores in the oil group were significantly higher than the casein group (P < 0.05) and trended toward being higher in the formula group (P = 0.085) at age 10 days. Total GSH activity was significantly higher in the sham groups than all ischemia groups on Day 10 (P < 0.001) and than the corn oil group on Day 35 (P < 0.05). GSH activity did not differ among ischemia groups. Conjugated diene concentrations were significantly higher in the casein group than the lactose and sham groups at age 10 days (P < 0.05) only. We conclude that intraluminal lipids may augment intestinal ischemic injury in the newborn (age 10 days) but not the weanling rat. While oxygen-free radicals were present during injury, lipid peroxidation from oxygen radicals was not responsible for this increase in histologic injury.
坏死性小肠结肠炎（NEC）主要在早产儿开始肠内喂养后发生。本研究的目的是评估肠腔内营养物质对NEC大鼠模型组织学损伤和氧化应激反应的影响。在出生后第10天和第35天，对Sprague-Dawley大鼠（共81只）进行剖腹手术。对照组仅接受假损伤。缺血组分别在肠腔内单次注射0.25 ml（第10天）或1.0 ml（第35天）的乳糖（8.6 g/dl）、酪蛋白（2.2 g/dl）、玉米油（4.4 g/dl）或婴儿配方奶粉（Similac；20 g/dl）。注射营养液后，缺血组进行肠系膜闭塞1小时，并在肠腔内注射血小板活化因子（50微克/千克）。6小时后或动物死亡时进行尸检。采集肠道样本进行组织学检查、测定总谷胱甘肽（GSH；一种抗氧化剂）和共轭二烯（一种脂质过氧化产物）。组织学损伤评分从0（正常）到5（透壁坏死）。在10日龄时，油组的显微镜下损伤评分显著高于酪蛋白组（P < 0.05），配方奶粉组的损伤评分呈升高趋势（P = 0.085）。在第10天，假手术组的总GSH活性显著高于所有缺血组（P < 0.001），在第35天，假手术组的总GSH活性显著高于玉米油组（P < 0.05）。缺血组之间的GSH活性没有差异。仅在10日龄时，酪蛋白组的共轭二烯浓度显著高于乳糖组和假手术组（P < 0.05）。我们得出结论，肠腔内脂质可能会加重新生大鼠（10日龄）而非断奶大鼠的肠道缺血性损伤。虽然损伤过程中存在氧自由基，但氧自由基引起的脂质过氧化并非组织学损伤增加的原因。
