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在肠腔内容物引发的坏死性小肠结肠炎模型中循环肠道脂肪酸结合蛋白的升高

Elevation of circulating intestinal fatty acid binding protein in a luminal contents-initiated model of NEC.

作者信息

Gollin G, Marks W H

机构信息

Department of Surgery, Yale University School of Medicine, New Haven, CT 06510.

出版信息

J Pediatr Surg. 1993 Mar;28(3):367-70; discussion 370-1. doi: 10.1016/0022-3468(93)90233-b.

Abstract

Necrotizing enterocolitis (NEC) continues to produce significant morbidity and mortality, due in part to the difficulty in detecting its initial manifestations at a stage when compromised intestine may potentially be salvaged. We have previously reported our findings that intestinal fatty acid binding protein (I-FABP) is a sensitive biochemical marker for early intestinal mucosal injury due to mesenteric ischemia. In this study we evaluated the potential of serum I-FABP as a marker for incipient NEC in a nonischemic model of NEC in the rat. Intraluminal instillation of a solution of casein (10 mg/mL) and calcium gluconate (50 mg/mL) in saline acidified to pH 4.0 with propionic acid resulted in a rapid and prolonged increase in serum I-FABP from a baseline of < or = 4.0 ng/mL to 171 +/- 40 ng/mL. Instillation of the same electrolyte solution with either casein or propionic acid alone resulted in a less dramatic elevation of serum I-FABP to 19 +/- 4 ng/mL and 76 +/- 30 ng/mL, respectively. In both cases baseline values of < or = 4.0 ng/mL were reached within 60 minutes. In control animals, which received saline alone, serum I-FABP was undetectable throughout the experiment. Simultaneously, we found that serum hexosaminidase, a putative biochemical marker for intestinal ischemia and NEC, was unchanged in all groups. Light microscopy of the intestinal specimens obtained three hours after instillation of casein and organic acid demonstrated superficial villus necrosis and villus blunting, but no areas of transmural necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

坏死性小肠结肠炎(NEC)仍然会导致严重的发病和死亡,部分原因在于在肠道受损可能得到挽救的阶段难以检测到其初始表现。我们之前曾报道过我们的研究结果,即肠脂肪酸结合蛋白(I-FABP)是肠系膜缺血所致早期肠黏膜损伤的敏感生化标志物。在本研究中,我们在大鼠非缺血性NEC模型中评估了血清I-FABP作为早期NEC标志物的潜力。向肠腔内滴注用丙酸酸化至pH 4.0的盐水中的酪蛋白(10 mg/mL)和葡萄糖酸钙(50 mg/mL)溶液,导致血清I-FABP从基线水平≤4.0 ng/mL迅速且持续升高至171±40 ng/mL。单独滴注含有酪蛋白或丙酸的相同电解质溶液,导致血清I-FABP分别升高至19±4 ng/mL和76±30 ng/mL,升高幅度较小。在这两种情况下,60分钟内均达到≤4.0 ng/mL的基线值。在仅接受盐水的对照动物中,整个实验过程中均未检测到血清I-FABP。同时,我们发现血清己糖胺酶(一种推测的肠道缺血和NEC生化标志物)在所有组中均未改变。滴注酪蛋白和有机酸三小时后获取的肠道标本的光学显微镜检查显示有浅表绒毛坏死和绒毛变钝,但无透壁坏死区域。(摘要截断于250字)

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