摘要
目的探讨细菌性腹膜炎大鼠小肠运动功能的变化及其机制。方法Wistar大鼠40只，随机分成对照组和实验组。实验组制作细菌性腹膜炎动物模型，观测两组大鼠小肠传输功能、小肠环行平滑肌肌条收缩能力、环行平滑肌细胞收缩反应及细胞内钙离子浓度的变化；测定小肠肌层诱导型一氧化氮合酶（iNOS）mRNA的表达量和平滑肌细胞培养基中一氧化氮含量的变化。结果实验组大鼠小肠传输较对照组明显延迟；对照组和实验组小肠环行肌条收缩力分别为（2．08±0．33）g／mm^2．s^-1、（0．75±0．06）g/mm^2．s^-1；平滑肌细胞收缩反应为（42．61±12．37）％、（11．42±4．23）％；钙离子浓度变化为（247±62）％、（119±21）％；实验组小肠肌层iNOS mRNA表达水平和平滑肌细胞培养基一氧化氮浓度较对照组显著升高（P〈0．05）。结论细菌性腹膜炎大鼠小肠运动功能障碍可能与小肠肌层iNOS mRNA过度表达产生大量一氧化氮，降低环行平滑肌细胞钙离子浓度有关。
Objective To explore the changes of intestinal motility and the mechanism in the rats with bacterial peritonitis. Methods Forty Wistar rats were divided into control and experimental group （ n = 20 in each group ）, and the latter was used to replicate bacterial peritonitis model. Gut transits were measured in vivo and intestinal circular muscle contractions were measured in an organ bath. The contractile response of dispersed circular smooth muscle cells and the changes of [ Ca^2 ＋ ] i stimulated by aceylcholine were measured. RT-PCR was used to detect the expression of inducible nitric oxide synthase （iNOS） mRNA within intestinal muscularis, and the level of nitric oxide （NO） in cell cultures was quantified. Results The gut transits in experimental group were obviously decreased as compared with control group. Circular smooth muscle contractility stimulated by aceylcholine in two groups was （2.08 ± 0.33） g/mm^2. s^-1 and （0.75 ± 0.06） g/mm^2. s^-1, contractile response of dispersed circular smooth muscle cells （42.61 ± 12.37）% and （ 11.42 ±4.23）% ,changes of [Ca^2＋ ]i responding to aceylcholine （247 ± 62） % and （ 119 ± 21 ） % respectively. Levels of iNOS mRNA expression were significantly elevated and NO production increased obviously （P 〈 0.05 ）. Conduslon Intestinal motility was weakened in bacterial peritonitis by reducing [ Ca^2＋ ] i which resulted from up-regulated expression of iNOS mRNA and the overproduction of NO within intestinal muscularis.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2007年第3期304-306,共3页
Chinese Journal of Experimental Surgery
