焦虑大鼠内脏敏感性增高以及行直结肠扩张后血清皮质酮的变化及意义

目的内脏高敏感性是肠易激综合征( 1BS)症状最重要的病理生理机制之一,焦虑可能与内脏高敏的发生密切相关。本研究旨在探讨焦虑对大鼠直结肠敏感性的作用以及血清皮质酮与内脏高敏的关系。方法Wistar大鼠随机分为对照组和焦虑组两组,通过对大鼠行空瓶刺激2周建立以焦虑为主要表现的慢性情绪应激模型。造模期间,观察大鼠的攻击、探究和修饰三种行为,对其进行情绪性行为学分析。造模结束后,以腹部回缩反射(AWR)评分为指标观察大鼠对直结肠气囊扩张(CRD)的反应性,评估内脏敏感性。然后将两组各随机分为扩张组和非扩张组,对扩张组行CRD ,并取血清,对血清皮质酮定量测定。结果空瓶刺激期间,同对照组相比,焦虑组探究、攻击行为明显增多,修饰行为减少(P <0 0 1)。焦虑组在2 0mmHg、40mmHg、60mmHg和80mmHg的扩张压力下的AWR评分均显著高于对照组(P <0 0 1)。焦虑组与对照组相比血清皮质酮水平明显升高(P <0 0 1) ,但各组扩张后皮质酮水平较扩张前仅有轻微升高,无显著差异(P >0 0 5 )。结论焦虑对IBS内脏高敏起一定作用,其发挥作用的机制可能并非单一通过下丘脑_垂体_肾上腺皮质系统(HPA轴)来实现,推测还可能与脑内单胺类神经递质NE浓度的改变有关。

Visceral hypersensitivity and the change of serum corticosterone level after colorectal distention in anxiety rats and their significance

Objective To investigate the role of anxiety in colorectal sensitivity in mice, and the correlation between serum corticosterone and visceral hypersensitivity.Methods Wistar rats were randomly divided into 2 groups, the control group and the anxiety group. A chronic emotional stress model of which main behavior was anxiety was established by empty bottle stimulation lasting 2 weeks. While the stressor was given, behavioral changes of rats including attack, explore and embellishment were observed and analysed. The visceral sensitivity to colorectal distention (CRD) was measured by abdominal withdrawal reflex scores (AWR scores). Then, each group was divided into CRD group and non_CRD group.The corticosterone content in serum was evaluated by radioimmunoassay.Results Compared with controls,attack and explore behaviors of anxiety rats manifolded, and embellishment decreased(P<0.01). AWR scores were significantly higher under all CRD pressures (20,40,60,80 mmHg) by stress,compared with controls(P<0.01). The level of corticosterone in serum significantly increased in anxiety rats, compared with controls(P<0.01).But in each anxiety group, the corticosterone content in CRD group wasn't significantly affected by CRD and only had a slight increase, compared with that non_CRD group (P>0.05).Conclusion Axiety has effects on visceral hypersensitivity in IBS. The mechanism may be not only due to differential activation of the HPA axis, and probably related with the NE concentration in brain.