The role of luminal nutrients in intestinal injury from mesenteric reperfusion and platelet-activating factor in the developing rat
The role of luminal nutrients in intestinal injury from mesenteric reperfusion and platelet-activating factor in the developing rat
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DOI：
10.1006/jsre.1996.0239
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发表时间：
1996-06-01
影响因子：
2.2
通讯作者：
Musemeche, CA
中科院分区：
文献类型：
--
作者：
Bhatia, AM;Feddersen, RM;Musemeche, CA
坏死性小肠结肠炎（NEC）主要发生在早产儿开始肠内喂养后。本研究的目的是评估肠内营养物质对NEC大鼠模型组织学损伤和氧化反应的影响。在出生后第10天和第35天，Sprague-Dawley大鼠（共n = 81）进行剖腹手术。对照组只接受假损伤。缺血组接受单次腔内注射0.25 ml（第10天）或1.0 ml（第35天）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，缺血组经肠系膜阻断1小时，腔内注射血小板活化因子（50 μ g/kg）。6小时后或死亡时进行尸检。采集肠道样本进行组织学、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）检测。组织学损伤评分从0（正常）到5（跨壁坏死）。10日龄时，油组显微损伤评分显著高于酪蛋白组（P < 0.05），配方组有升高趋势（P = 0.085）。假手术组总谷胱甘肽活性在第10天显著高于各缺血组（P < 0.001），第35天显著高于玉米油组（P < 0.05）。GSH活性在缺血组间无差异。10日龄时，酪蛋白组共轭二烯浓度仅显著高于乳糖组和假药组（P < 0.05）。我们的结论是，腔内脂质可能会增加新生儿（10日龄）的肠道缺血性损伤，但对断奶大鼠没有影响。虽然损伤期间存在氧自由基，但氧自由基引起的脂质过氧化并不是造成组织学损伤增加的原因。(C) 1996学术出版社，Inc.
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 mu g/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 mere 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. (C) 1996 Academic Press, Inc.