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目的将新生Wistar大鼠进行缺氧、低温、鼠乳代用品人工喂养、不同剂量脂多糖(LPS)灌胃等综合因素刺激,造成坏死性小肠结肠炎(NEC),并导致全身炎症反应综合征(SIRS)的动物模型。方法 40只新生Wistar大鼠,出生36～48h随机分成4组,每组各10只。A组为正常对照组,B、C、D组采用低温缺氧(给予1 L.L-1氮气缺氧90s,4℃冷刺激10 min,每天2次,连续2 d)、鼠乳代用品人工喂养、不同剂量LPS(5 mg.kg-1、10 mg.kg-1、20 mg.kg-1)灌胃。实验结束后处死动物,HE染色光镜下观察其回盲部近端肠组织形态学改变,采用肠损伤病理评分进行评价,组织学评分≥2分确定为NEC,根据血液白细胞总数及呼吸改变确定为SIRS。结果 B、C、D组大鼠逐渐出现腹泻、腹胀、活动减少,D组大鼠50%发生死亡。A、B、C、D4组肠损伤病理评分分别为(0.33±0.10)分、(2.03±1.16)分、(3.77±0.41)分、(3.13±0.69)分,组间差异有统计学意义(H=29.83,P<0.01)。NEC发病率分别为0%、50%、100%和100%;SIRS发生率分别为0%、30%、70%和70%。结论在鼠乳代用品人工喂养、缺氧低温刺激条件下,给予LPS灌胃可诱导新生鼠发生NEC,并导致SIRS发生,本模型与新生儿SIRS病理改变接近,是一种比较理想的研究新生儿SIRS的动物模型。
OBJECTIVE: To investigate the effects of hypoxia, hypothermia, artificial feeding on mouse milk substitutes, and intragastric administration of lipopolysaccharide (LPS) at different dosages to induce necrotic enterocolitis (NEC) in neonatal Wistar rats and to induce systemic inflammatory response syndrome (SIRS) animal model. Methods Forty freshmen Wistar rats were randomly divided into four groups (n = 10). Group A was normal control group, Group B, C, D hypothermia hypoxia (1 LL-1 nitrogen hypoxia 90s, 4 ℃ cold stimulation 10 min, 2 times a day for 2 consecutive days), mouse milk substitute artificial feeding , Different doses of LPS (5 mg.kg-1, 10 mg.kg-1, 20 mg.kg-1) intragastrically. Animals were sacrificed at the end of the experiment. Morphological changes in the proximal ileum of the ileocecal part were observed under light microscope. The pathological score of intestinal injury was used to evaluate the histological score. The score of histological score ≥2 was determined as NEC, which was determined according to the total number of leukocytes and respiration For SIRS. Results B, C and D rats gradually developed diarrhea, abdominal distension and decreased activity, and 50% of rats in group D died. The pathological scores of intestinal injury in groups A, B, C and D4 were (0.33 ± 0.10) points, (2.03 ± 1.16) points, (3.77 ± 0.41) points and (3.13 ± 0.69) points respectively. There was significant difference between the groups H = 29.83, P <0.01). The incidence of NEC was 0%, 50%, 100% and 100% respectively; the incidence of SIRS was 0%, 30%, 70% and 70% respectively. CONCLUSIONS: LPS can induce NEC and induce SIRS in rats fed with LPS under artificial hypoxia and hypoxia stimulation. This model is similar to neonatal SIRS pathological changes and is an ideal freshmen Animal models of SIRS.