摘要
目的 肠道是新生儿窒息后受损最严重的器官之一。但目前国内外尚无一经典模型用于窒息后 肠道损伤的研究。本研究采用可逆性宫内缺血制作了大鼠窒息后肠道损伤模型。方法 钳夹足月孕鼠(E21)一 侧子宫和卵巢动静脉20min,以结扎侧的胎鼠为窒息组,对侧胎鼠为对照组。剖宫产取出胎鼠,复苏,代乳鼠代乳。 分别饲养0,24,48,72h后处死(每组每时点18只),取出肠组织行病理观察,评估肠黏膜损害指数(IMDI)。结果 对照鼠娩出后表现正常;缺血鼠娩出后出现皮肤青紫、呼吸减弱、四肢活动减少等窒息改变。缺血鼠病理学改变在 缺血后48h最重,IMDI明显上升(3.40±0.16),对照组肠粘膜几乎没有损害(0.00±0.00)。缺血后72h肠道损 伤明显恢复,IMDI降至0.60±0.21。结论 钳夹足月孕鼠一侧子宫、卵巢动静脉可以制成窒息后肠道损伤的动 物模型。
Objective The intestine is one of the most seriously injured organs during neonatal asphyxia. But a model for studying the perinatal intestinal injury caused by asphyxia is absent. This paper described a model of intestinal damage produced by reversible intrauterine ischemia in rats. Methods The model of acute reversible intrauterine ischemia was established by clamping the arteries and veins on one side of the uterus and ovaries in pregnant Wistar rats (E21) for 20 minutes. The fetal rats on the occluded side of the uterus were used as the Ischemia group and the rats on the other side were used as the Control group. After 20 minutes of vascular occlusion, the uteri were opened and the pups were removed. In each group, 18 pups were sacrificed at 0, 24, 48 and 72 hrs after ischemia, respectively. The intestinal mucosal damage index (IMDI) was evaluated. Results After ishemia, the pups in the Ischemia group were cyanotic or pale, listless, and hypopneic, while the control pups manifested normal. The intestinal mucosa of controls were not damaged. In the Ischemia group, intestinal damage reached a peak at 48 hrs post-ischemia, with an IMDI that was significantly increased above controls (3.40±0.16 vs 0.00±0.00, P<0.01). At 72 hrs post-ischemia, the changes of intestinal tissues had largely recovered and the IMDI decreased to 0.60 ± 0.21. Conclusions The animal model of asphyxia induced perinatal intestinal injury can be established by clamping the arteries and veins on one side of the uterus and ovaries in pregnant rats.
出处
《中国当代儿科杂志》
CAS
CSCD
2005年第1期12-14,共3页
Chinese Journal of Contemporary Pediatrics
基金
SupportedbytheGrantofScienceandTechnologyofLiaoningProvince(No.20122166).