CAJ | 학술논문

目的观察小肠潘氏细胞在大鼠失血性休克复苏后肠黏膜重建过程中的作用。方法 42只雄性Wistar大鼠建立失血性休克复苏模型,随机分为实验组(n=7)和对照组(n=35),实验组再分5组,分别于复苏后1、3、6、12、24h观察回肠黏膜的形态学改变、复苏前后潘氏细胞数量及形态变化特点及各时相电镜下潘氏细胞结构特点。结果休克复苏后小肠黏膜明显损伤,集中表现于绒毛部分。复苏后3h为明显,6h后绒毛已开始修复,至24h肠黏膜表面细胞连续性已恢复。复苏后1h,回肠黏膜潘氏细胞计数明显减少(P＜0.05),3h降至最低(P＜0.05),6h后与对照组比较,差异无统计学意义(P＞0.05)。电镜下潘氏细胞表现肠内分泌细胞超微结构特征,核无凋亡改变。结论失血性休克复苏后肠黏膜屏障早期受损,但具快速重建能力,潘氏细胞颗粒的合成和分泌可受缺血再灌注损伤的诱导。潘氏细胞对维持肠道黏膜防御机制具有重要的生理意义。
목적 관찰소장반씨세포재대서실혈성휴극복소후장점막중건과정중적작용。방법 42지웅성Wistar대서건립실혈성휴극복소모형,수궤분위실험조(n=7)화대조조(n=35),실험조재분5조,분별우복소후1、3、6、12、24h관찰회장점막적형태학개변、복소전후반씨세포수량급형태변화특점급각시상전경하반씨세포결구특점。결과 휴극복소후소장점막명현손상,집중표현우융모부분。복소후3h위명현,6h후융모이개시수복,지24h장점막표면세포련속성이회복。복소후1h,회장점막반씨세포계수명현감소(P＜0.05),3h강지최저(P＜0.05),6h후여대조조비교,차이무통계학의의(P＞0.05)。전경하반씨세포표현장내분비세포초미결구특정,핵무조망개변。결론 실혈성휴극복소후장점막병장조기수손,단구쾌속중건능력,반씨세포과립적합성화분비가수결혈재관주손상적유도。반씨세포대유지장도점막방어궤제구유중요적생리의의。
Objective To investigate the changes of Paneth cells during the restitution process of intestinal mucosa after hemorrhagic shock in rats. Methods A total of 42 Wistar male rats were randomized divided into control group ( n =7) and model group ( n =35 ). The rats in model group were further divided into five subgroups (n =7 in each group) according to different time points. Hemorrhagic shock model was established. The morphological changes of ileum mucosa and Paneth cells were observed during the restitution process after hemorrhagic shock, and the number of Paneth cells was counted under the light microscopy at different time points. Ultrastructures of Paneth cells were observed under different stages of resuscitation. Results After hemorrhagic shock, the mucosal epithelial injury was obvious in the upper villus and became more serious in 1 h up to 3 h, and mucosal restitution was found 6 h after resuscitation, almost established within 24 h. The number of Paneth cells in the intestinal mucosa was reduced significantly at 1 h after restitution (P ＜ 0. 05 ), reached the lowest at 3 h (P ＜ 0. 05 ), and gradually increased from 6 h after restitution (P ＞ 0. 05). Paneth cells showed ultrastructural features of intestinal endocrine cells.No apoptotic nuclear change was found. Conclusion Intestinal mucosa barrier was subjected to injury in the early stage of reperfusion after hemorrhagic shock, but it could recover rapidly. The synthesis and secretion of Paneth cell granules could be induced by ischemia-reperfusion injury of small intestine. Paneth cells played an important role in defensive mechanism of intestinal mucosa.