肠道炎症诱导的内脏和躯体痛觉过敏

摘要

背景:慢性腹痛是功能性胃肠病患者常见症状之一,此类患者亦可同时具有较明显的躯体症状.内脏和躯体症状并存极大影响了患者的生活质量,并增加就医负担.目的:观察肠道炎症后大鼠内脏和躯体痛觉,探究两者间的联系和可能的共同发病机制.方法:80只雄性Sprague-Dawley大鼠随机分为模型组、溶剂对照组和阴性对照组,分别给予20 mg TNBS/乙醇混合液、50％乙醇和0.9％ NaCl溶液灌肠.灌肠8周后,行不同压力结直肠扩张(CRD)诱导内脏运动反射(VMR)以评估大鼠内脏痛觉.以机械缩足反射阈值(MWT)和甩尾反射潜伏期(TFL)评估躯体痛觉.结果:造模8周后模型组大鼠结肠黏膜病理表现与两组对照组相比无明显差异,未见明显溃疡和炎性细胞浸润.与两组对照组相比,32.5％的模型组大鼠内脏痛觉阈值明显下降(P＜0.001),且这部分内脏痛觉高敏感的模型组大鼠MWT和TFL均明显降低(P＜0.001).结论:本研究建立的动物模型模拟了感染后肠易激综合征状态,TNBS诱导的肠道炎症同时导致了大鼠内脏和躯体痛觉过敏,有助于进一步探究内脏和躯体痛觉过敏的共同发病机制.%Chronic abdominal pain is one of the most common symptoms in patients with functional gastrointestinal disorders (FGIDs). These patients also exhibit some somatic symptoms, Comorbid visceral and somatic symptoms greatly influence the patient' s quality of life and increase the burden of medical resources. Aims: To observe visceral and somatic pain sensation after intestinal inflammation in rats to explore the relationship between and common pathogenesis of these symptoms, Methods; Eighty Sprague-Dawley male rats were randomly divided into model group, solvent control group and negative control group; thereafter 20 mg TNBS/ethanol mixture, 50% ethanol and saline were infused by enema, respectively. Eight weeks after enema, visceromotor responses (VMR) in response to graded colorectal distention (GRD) was recorded to evaluate visceral pain sensation. Mechanical withdrawal threshold (MWT) and tail flick latency (TFL) were used to evaluate somatic pain sensation. Results; No ulcer and inflammatory cell infiltration was found in colon mucosa in TNBS-treated rats eight weeks after establishment, and no significant difference in pathology was found among the three groups, Compared with two control groups, 32. 5% model rats presented lowered visceral pain perception threshold (P<0.001) , and these visceral hypersensitivity rats also showed significantly decreased MWT and TFL (P < 0, 001). Conclusions; The animal model mimicked the pain sensation situation of post-infectious irritable bowel syndrome. Visceral and somatic hypersensitivity are caused by TNBS-induced intestinal inflammation. This will help for further exploring the common pathogenesis of visceral and somatic hypersen&itivity.