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作 者:唐明贵[1] 王印华[1] 王宝华[1] 浦践一[1] 邱方 李志强[1]
机构地区:[1]河北联合大学附属医院ICU,河北省唐山市063000 [2]秦皇岛第一医院ICU,河北省秦皇岛市066000
出 处:《世界华人消化杂志》2014年第21期3161-3165,共5页World Chinese Journal of Digestology
基 金:唐山市科技局基金资助项目;No.13130284z~~
摘 要:目的:研究早期肠内给予卡巴胆碱对弥漫性颅脑损伤后大鼠肠机械屏障的影响.方法:采用Marmarou模型制备方法造成成年雄性Wistar大鼠弥漫性颅脑损伤,造模后成活的大鼠随机分为生理盐水组(NS组,n=40)及卡巴胆碱组(CAR组,n=40),另设只切开头皮的假手术组(对照组,n=25).对照组自由饮水,NS组及CAR组从造模成功后2 h开始灌胃,分别给予生理盐水及卡巴胆碱[100μg/(kg?12 h)],于伤后3、6、12、24、48 h活杀取材,检测血浆中二胺氧化酶(daimine oxidase,DAO)活性、D-乳酸含量及小肠绒毛病理学改变.结果:成功复制弥漫性颅脑损伤大鼠模型,弥漫性颅脑损伤后大鼠肠黏膜固有层水肿,炎性细胞浸润,部分黏膜上皮细胞变性、坏死、脱落,绒毛变短,在12 h损伤最重,24 h肠黏膜有增高趋势,CAR组肠绒毛较NS组恢复快,至48 h肠绒毛高度未恢复至对照组水平,但无统计学差异.弥漫性颅脑损伤后血浆中DAO活性及D-乳酸含量较对照组显著升高(P<0.01),至伤后48 h未恢复至对照组水平(P<0.01).CAR组血浆中DAO活性及D-乳酸含量在伤后3-48 h低于NS组,除3 h D-乳酸含量降低无统计学意义外均有统计学意义(P<0.05).结论:弥漫性颅脑损伤后早期肠内给予卡巴胆碱能减轻肠黏膜损伤,对肠黏膜机械屏障有一定的保护作用.AIM: To investigate the effect of early intestinal carbachol supplementation on intestinal muco- sal barrier in rats after diffuse brain injury (DBI). METHODS: A male adult Wistar rat model of DBI was established by the Marmarou's method. Injured and survived rats were randomly divid- ed into either a normal saline group (NS group, n = 40) or a carbachol group (CAR group, n = 40). Normal saline and carbachol [100 gg/(kg·12 h)] were intragastrically given to animals of the NS and CAR groups 2 h after injury, respec- tively. Meanwhile, a sham operation group (n = 25) was also included. All animals were sacri- ficed at 3, 6, 12, 24, 48 h after DBI to determine the activity of plasma DAO and concentration ofplasma D-lactate, and to observe intestinal villus changes by microscopy. RESULTS: DBI was reproduced successfully in rats. Edema of the lamina propria, infiltration of inflammatory cells, degeneration and necrosis of mucosal epithelial cells were most serious at 12 h after DBI induction. The height of intestinal villi had an increasing tendency from 24 h, and intestinal villous changes recovered more sig- nificantly at 48 h in the CAR group than in the control group (P 〉 0.05). The activity of DAO and the content of D-lactate in plasma increased obviously in rats after DBI (P 〈 0.01), while they did not recover to the level of the sham-opera- tion group at 48 h (P 〈 0.01). Both the activity of DAO and the content of D-lactate in plasma were significantly lower in the CAR group than in the NS group, except for the content of D-lac- tate at 3 h after injury (P 〈 0.05). CONCLUSION: Early intestinal carbachol sup- plementation can alleviate intestinal mucosal damage and has an appreciable protective effect on intestinal mucosal mechanical barrier in rats after DBI.
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