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目的观察急性肝衰竭大鼠胃肠消化间期移行性复合运动的变化与肠神经元的关系。方法采用D-氨基半乳糖诱导的急性肝衰竭大鼠模型,使用多道生理记录仪记录正常大鼠和急性肝衰竭大鼠的胃肠消化间期移行性复合运动,采用TUNEL法、5-HT和NSE免疫组化法检测空肠神经元的凋亡情况。结果急性肝衰竭大鼠空肠MMC周期较对照组显著延长(1897.71±815.77对1384.17±449.34S,P<0.05),尤以Ⅱ期延长为主(1870.90±1010.35S对643.04±450.67S,P<0.05),成簇状移行性收缩,Ⅲ期显著缩短(31.41±11.17S对53.11±14.74S,P<0.05);急性肝衰竭大鼠肠神经元凋亡明显增多,TUNEL染色阳性细胞核固缩或碎裂,呈棕黄色,细胞大小不一;5-HT和NSE免疫组化检测发现急性肝衰竭大鼠阳性物质表达较正常大鼠减少。结论急性肝衰竭大鼠胃肠MMCⅡ期延长,Ⅲ期明显缩短,导致胃肠动力异常,可能与肠神经元的凋亡有关。
Objective To observe the relationship between the changes of intestine and intestine neurons during the gastrointestinal interdynamic transitional motility in rats with acute hepatic failure. Methods Acute hepatic failure induced by D-galactosamine in rats was used to record the gastrointestinal interdynamic transitional motility in normal rats and acute hepatic failure rats using multi-channel physiology recorder. TUNEL, 5-HT And NSE immunohistochemistry to detect the apoptosis of jejunum neurons. Results The jejunal MMC cycle of rats with acute hepatic failure was significantly longer than that of the control group (1897.71 ± 815.77 vs 1384.17 ± 449.34S, P <0.05), especially in the prolonged period of Ⅱ (1870.90 ± 1010.35S vs. 643.04 ± 450.67S, P <0.05 ), Cluster-like migratory contractions, and phase Ⅲ significantly shortened (31.41 ± 11.17S vs 53.11 ± 14.74S, P <0.05). Apoptosis of the intestine neurons in acute hepatic failure rats was significantly increased, and nuclear staining of TUNEL positive cells Cracked, brownish yellow, cell size varies; 5-HT and NSE immunohistochemical detection of acute liver failure rat positive expression decreased compared with normal rats. Conclusions Acute liver failure rats with prolonged stage Ⅱ Ⅱ MMCII, Ⅲ significantly shortened, leading to gastrointestinal motility abnormalities may be related to apoptosis of intestinal neurons.