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探讨镁缺乏对小肠形态和功能的影响。将雄性SD大鼠分为4组,分别给予镁过量或镁缺乏食物1～3周,小肠病理切片观察中性粒细胞浸润和肠粘膜的损伤程度。镁单独缺乏可诱导中性粒细胞浸润增加和血管内皮细胞-1表达的上升,但不引起肠粘膜损伤及促炎介质的表达,镁缺乏伴随着分泌型上皮细胞反应和血管大分子渗漏到小肠和肺组织。实验动物随机施行假手术,或肠系膜上动脉闭塞10min到30min,随后进行1h或4h的再灌注。少数大鼠表现出大量的多型核白细胞聚集。肠缺血后再灌注4h导致血管大分子渗漏入小肠和肺组织。实验表明,镁缺乏导致小肠的亚临床炎症反应,不伴有粘膜的损伤,但却伴随着局部和远处器官功能上的改变,同时也提高了对于氧化应激的敏感性。
To investigate the effect of magnesium deficiency on the morphology and function of small intestine. The male SD rats were divided into 4 groups and were given magnesium excess or magnesium deficiency for 1 to 3 weeks respectively. Pathological sections of small intestine were observed for neutrophil infiltration and injury of intestinal mucosa. Lack of magnesium alone induces an increase in neutrophil infiltration and an increase in vascular endothelial cell-1 expression but does not cause intestinal mucosal injury and pro-inflammatory mediators, and magnesium deficiency is accompanied by secretory epithelial cell responses and vascular macromolecule leakage Small intestine and lung tissue. The animals were randomized to either sham surgery or occlusion of the superior mesenteric artery for 10 min to 30 min followed by 1 or 4 h reperfusion. A few rats showed a large number of polymorphonuclear leukocyte accumulation. Intestinal ischemia and reperfusion 4h lead to leakage of vascular macromolecules into the small intestine and lung tissue. Experiments have shown that magnesium deficiency causes subclinical inflammatory reactions in the small intestine without mucosal damage but with functional changes in both local and distant organs and increased susceptibility to oxidative stress.