迷走神经背核毁损对急性食管炎模型大鼠食管下括约肌压力影响的研究

Destruction of the dorsal motor nucleus of the vagus affects lower esophageal sphincter pressure in acid-induced acute esophagitis in a rat model

目的探讨迷走神经背核毁损对急性食管炎模型大鼠食管下括约肌压力的影响。方法将40只雄性SD大鼠数字抽签随机分为4组(每组10只),分别为对照组、迷走神经背核假毁损(假毁损组)、迷走神经背核毁损(毁损组)、迷走神经背核毁损后迷走神经刺激(毁损后刺激组)。迷走神经背核毁损/假毁损两周后,给予大鼠食管胃交界处滴注盐酸胃蛋白酶溶液90 min,分别于迷走神经背核毁损/假毁损前、后及滴注盐酸胃蛋白酶溶液结束60 min后行食管下括约肌压力测定,对照组直接测定。手术后毁损刺激组大鼠在食管滴酸前15 min和结束后15 min予电流刺激左侧迷走神经干30 min。滴注结束60 min后处死动物。取食管下段组织观察食管炎症程度及炎症因子表达情况。结果毁损组大鼠两周后食管下括约肌压力较前下降(34.0±8.9)cmH2O比(25.9±8.8)cmH2O(P<0.05),滴注盐酸胃蛋白酶结束60 min后食管下括约肌压力较前下降(18.6±3.6)cmH2O(P<0.01);毁损后刺激组大鼠食管下括约肌压力升高(22.3±2.9)cmH2O比(18.6±3.6)cmH2O(P<0.05);两周后假毁损组大鼠食管下括约肌压力无明显变化,滴注盐酸胃蛋白酶溶液结束60 min后食管下括约肌压力升高(30.0±9.5)cmH2O比(37.8±5.8)cmH2O(P<0.05)。毁损组大鼠食管下段炎症较假毁损组大鼠食管下段炎症加重(P<0.01),炎症因子肿瘤坏死-α、白细胞介素(IL)-6、IL-1β、前列腺素E2表达增加(P<0.01);迷走神经刺激后食管下段炎症及炎症因子表达下降(P<0.01)。结论迷走神经背核毁损导致食管下括约肌压力下降,加重急性食管炎模型大鼠食管炎症与损伤,迷走神经刺激可加强食管下括约肌压力,改善食管下段炎症。

Objective To investigate the impact of the destruction of dorsal motor nucleus of the vagus(DMV)0n lower esophageal sphincter pressure in a rat model of acute esophagitis.Methods A total of 40 male Sprague-Dawley(SD)rats were randomly divided into four groups:the control group,sham group,DMV destruction group,DMV destruction+vagal stimulation group.Two weeks after DMV destruction or sham operation,hydrochloric acid with pepsin was perfused into the esophagogastric junction of rats for 90 min,and lower esophageal sphincter pressure was measured before and after operation and 60 min after acid perfusion.Rats in the control group received assessment of lower esophageal sphincter pressure directly.Rats in the DMV destruction vagus stimulation group were given electric current stimulation for 30 minutes before and after 15 min of esophageal acid perfusion.Rats were sacrificed after 60 min of the acid perfusion.The esophagus was prepared for hematoxylin and eosin(HE)staining,and the degree of inflammation and the expression of inflammatory cytokines were examined.Results In the DMV destruction group,lower esophageal sphincter pressure decreased 2 weeks after DMV destruction compared with pre-destruction levels(25.9±8.8 cmH20 vs.34.0 ± 8.9 cmH2 O,P 0.05),and lower esophageal sphincter pressure decreased after 60 min of acid perfusion compared with pre-destruction levels(18.6± 3.6 cmH2 O vs.25.9±8.8 cmH20,P<10.01).In the DMV destruction+vagus stimulation group,lower esophageal sphincter pressure increased after vagus nerve stimulation(22.3±2.9 cmH20 vs.18.6 ± 3.6 cmH2O)(P<O.05).There was no significant difference in lower esophageal sphincter pressure in the sham group before and after sham operation,while the pressure increased after acid perfusion(30.0±9.5 cmH20 vs.37.8±5.8 cmH2O,P<0.05).The degree of inflammation in the lower esophagus was aggravated and the expression of tumor necrosis factor-a,interleukin(IL)-6,IL-1β and prostaglandin E2 in esophageal tissues increased in the DMV destruction group compared with the sham group(P<0.01).The inflammation degree and the expression of inflammatory factors in the lower esophagus improved after vagal nerve stimulation compared with pre-stimulation levels(P< 0.01).Conclusions DMV destruction decreases lower esophageal sphincter pressure and aggravates esophageal inflammation and injury in a rat model of acute esophagitis.Vagus nerve stimulation can strengthen the pressure of the lower esophageal sphincter and improve the inflammation of the lower esophageal segment.