Naveh Y, Shalata A, Shenker L, Coleman R
Department of Pediatrics, Rambam Medical Center, Haifa, Israel.
Biometals. 2000 Mar;13(1):29-35. doi: 10.1023/a:1009205505217.
Inflammatory conditions of the gastrointestinal tract and iron-deficiency anemia are very common in humans. Acute intestinal inflammation was pathologically established in rats by intraluminal administration of acetic acid into the duodenum and the proximal jejunum. The study included two control groups of intact (untreated) rats and sham-operated (saline-treated) rats for each intestinal segment. A third group of rats received acetic acid. The acetic acid-induced inflammatory process was established histopathologically and biochemically. Two days after treatment, iron absorption was measured using ligated 10-cm loops of proximal jejunum or ligated duodenum in which 59Fe was injected intraluminally (n = 6 in each group). In another four control groups (intact and sham-operated for each intestinal segment) and two acetic acid-treated groups, serosal-luminal secretion of 59Fe was measured after intravenous injection (n = 5 in each group). 59Fe transfer from the lumens of the duodenum and jejunum to the portal system was significantly lower in those rats in whom inflammation was induced by acetic acid. There was no apparent serosal-luminal secretion of intravenously injected 59Fe in any of the studied groups. We conclude that acetic acid-induced intestinal inflammation significantly reduces iron absorption by the duodenum and the proximal jejunum.
胃肠道的炎症性疾病和缺铁性贫血在人类中非常常见。通过向十二指肠和空肠近端腔内注入乙酸,在大鼠身上建立了急性肠道炎症的病理模型。该研究包括针对每个肠段的两组完整(未处理)大鼠和假手术(生理盐水处理)大鼠作为对照组。第三组大鼠接受乙酸处理。通过组织病理学和生物化学方法确定了乙酸诱导的炎症过程。处理两天后,使用结扎的10厘米近端空肠环或结扎的十二指肠测量铁吸收,其中向腔内注射59Fe(每组n = 6)。在另外四个对照组(每个肠段的完整组和假手术组)和两个乙酸处理组中,静脉注射后测量59Fe的浆膜-腔内分泌(每组n = 5)。在那些由乙酸诱导炎症的大鼠中,59Fe从十二指肠和空肠腔向门静脉系统的转移显著降低。在任何研究组中,静脉注射的59Fe均未出现明显的浆膜-腔内分泌。我们得出结论,乙酸诱导的肠道炎症显著降低了十二指肠和近端空肠对铁的吸收。