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作 者:刘丽[1] 吴文斌[1] 周慧[1] 李桂香[1] 魏磊[1] 邹多武[1] 高峻[1] 李兆申[1]
机构地区:[1]第二军医大学附属长海医院消化内科,200433
出 处:《国际消化病杂志》2010年第5期307-310,共4页International Journal of Digestive Diseases
摘 要:目的观察出血性休克(HS)对大鼠小肠推进率和离体小肠收缩活动的影响以及此病程中肠神经的变化。方法将52只雄性SD大鼠随机分为对照组(n=26)和HS组(n=26)。HS组在给予重度出血性休克后行复苏,对照组大鼠给予相同麻醉及插管,但不行休克。复苏6h后处死大鼠。两组大鼠处死前30min伊文斯蓝灌胃测定小肠推进率;检测离体空肠自发收缩活动及对河豚毒素(TTX)的收缩反应;观察两组肠肌间神经丛(MP)中PGP9.5免疫荧光染色的差异。结果 HS组小肠推进率明显低于对照组(P<0.05)。与对照组相比,HS组离体空肠自发收缩的振幅显著降低(P<0.05)。加入TTX后,对照组空肠自发收缩的曲线下面积显著降低(P<0.05),而在HS组则无显著变化。与对照组相比,HS组MP中PGP9.5的阳性面积(P<0.05)及累积光密度(P<0.05)均显著降低。结论 HS可损伤大鼠小肠动力功能,MP中肠神经元的破坏可能是造成肠道运动功能障碍的神经源性机制。Objective Our aim was to investigate the effect of hemorrhagic shock (HS) on the enteric motor function and the alteration of myenteric neurons in a rat model. Methods Fifty-two Sprague-Dawley rats were randomly divided into control group (n = 26) and HS group (n = 26). HS group rats were subjected to severe hemorrhagic shock followed by resuscitation. Control group rats underwent cannulation and anesthesia for an identical period of time as shock animals but were not bled. Both HS group and control group were killed at 6 h after resuscitation. Rats in each group were gavaged with Evans blue, and then the transmission of Evans blue in small intestine was determined. Jejunum segments were used to observe changes in spon-taneous contractions and contractile response to TTX. The spreading specimens of intestinal myenteric plexus (MP)of jejunum were prepared and the myenteric neurons immunoreactive cells were evaluated using the marker of PGP 9.5. Results The propellant velocity of Evans blue was slower in HS group than the control group (P〈0.05). The amplitude of jejunum spontaneous contractions significantly decreased (P〈0.05) in the HS group compared with the control group. The area under curve of spontaneous contractions after TTX treatment declined significantly in control group(P〈0. 05), but not in HS group. The positive area and integrated optical density of the myenteric neurons per field significantly decreased (P〈0.05) in the HS group compared with the control group. Conclusions Our result suggested that intestinal motility is impaired in a rat model of HS and the deficiencies in myenteric nerves may be a underlying mechanism of the intestinal motor dysfunction.
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