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作 者:杭春华[1] 史继新[1] 黎介寿[2] 吴伟[1]
机构地区:[1]南京军区南京总医院神经外科 [2]南京军区南京总医院解放军普通外科研究所,江苏南京210002
出 处:《肠外与肠内营养》2005年第2期94-98,共5页Parenteral & Enteral Nutrition
摘 要:目的:探讨创伤性脑损伤后肠黏膜形态和屏障功能的变化,了解肠黏膜屏障功能障碍的发生时间及其严重程度。 方法:雄性Wistar大鼠随机分为无脑损伤的对照组和脑损伤后 3、12、24、72h和 7天组,每组 6只。应用组织病理和电镜观察肠黏膜结构的变化,通过测定血浆内毒素水平和肠黏膜通透性,以评价肠黏膜屏障功能。 结果:创伤性脑损伤后 3h即出现肠黏膜的病理改变,然后逐渐加重。与对照组相比,脑损伤后 3、12和 24h血浆内毒素水平明显升高,伤后 72h达到高峰,第 7天开始下降。血浆内毒素水平在伤后 3h和 72h出现两个峰值。脑损伤后肠黏膜通透性明显增加。 结论:创伤性脑损伤后 3h即可引起明显的肠黏膜结构和屏障功能损害,至伤后 72h达高峰,此损害可持续 7天以上。Objectives: The aim of the current study was to explore the alterations of intestinal mucosa morphology and barrier function, and to determine how rapidly impairment of gut barrier function occurs and how long it persists following traumatic brain injury. Methods: Male Wistar rats were randomly divided into six groups (6 rats each group) including controls without brain injury and traumatic brain injury groups at hours 3, 12, 24, 72 and days 7. The intestinal mucosa structure was detected by histopathological examination and electron microscopy. Gut barrier dysfunction was evaluated by detecting serum endotoxin and intestinal permeability. The level of serum endotoxin and intestinal permeability were measured by using chromogenic limulus amebocyte lysate and lactulose/mannitol (L/M) ratio, respectively. Results: After traumatic brain injury, the histopathological alterations of gut mucosa occurred rapidly as early as 3 hours and progressed to a serious state, including shedding of epithelial cells, fracture of villi, focal ulcer, fusion of adjacent villi, dilation of central chyle duct, mucosal atrophy, and vascular dilation, congestion and edema in the villous interstitium and lamina propria. Apoptosis of epithelial cells, fracture and sparseness of microvilli, loss of tight junction between enterocytes, and damage of mitochondria and endoplasm were found by electron microscope. The villous height, crypt depth and surface area in jejunum decreased progressively with the time of brain injury. The level of serum endotoxin and L/M ratio were significantly higher in traumatic brain injury groups than that in control (P< 0.01 ). Two peaks of serum endotoxin were found at hours 3 and 72 following brain injury. Conclusions: Traumatic brain injury can induce significant damage of gut structure and barrier function.
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