Etus Volkan, Tugay Melih, Utkan Tijen, Muezzinoglu Bahar, Ceylan Savas
Department of Neurosurgery, Kocaeli University, Kocaeli, Turkey.
J Surg Res. 2004 May 15;118(2):197-202. doi: 10.1016/j.jss.2004.01.007.
An association between hydrocephalus and gastroesophageal motor abnormalities that cause gastroesophageal reflux (GER) is well known. Our aim was to investigate hydrocephalus-induced alterations in esophageal and gastric smooth muscle reactivity and their modulation by pharmacological interventions in the rat model.
Hydrocephalus was induced in infantile rats by injection of kaolin into the cisterna magna. Hydrocephalic and sham-operated rats were exsanguinated 2 weeks after surgery. Esophageal and gastric fundus smooth muscle strips were studied in vitro for their contractile and relaxant response to receptor activation in the organ chambers set up. Additionally, esophageal and gastric tissue specimens were examined histologically for GER-induced changes.
No histological evidence of esophageal and gastric changes reflecting GER was observed in the specimens of the control and hydrocephalus-induced rats. Maximum contractile responses of esophageal and gastric fundus smooth muscle to KCl and muscarinic receptor agonist carbachol were increased in the hydrocephalic groups compared with the control groups. These changes were statistically significant. Relaxant responses to beta adrenoceptor agonist isoprenaline were similar in the esophageal muscle strips of both hydrocephalic groups and the control groups. However, isoprenaline-induced relaxant responses of the gastric fundus muscle strips in the hydrocephalus-induced groups were significantly decreased as compared with the control groups. The relaxant responses to papaverine in the esophageal and gastric fundus smooth muscle strips were similar in the two groups.
Our study revealed alterations of receptor-dependent and receptor-independent foregut smooth muscle reactivity in the hydrocephalus-induced rat pups. Therefore, we suggest that impaired smooth muscle reactivity at least in part may contribute to abnormalities of foregut motor function seen in patients with hydrocephalus.
脑积水与导致胃食管反流(GER)的胃食管运动异常之间的关联已广为人知。我们的目的是在大鼠模型中研究脑积水引起的食管和胃平滑肌反应性改变以及药物干预对其的调节作用。
通过向幼鼠的大池内注射高岭土诱导脑积水。脑积水大鼠和假手术大鼠在术后2周放血处死。在体外研究食管和胃底平滑肌条对所设置器官腔内受体激活的收缩和舒张反应。此外,对食管和胃组织标本进行组织学检查,以观察GER引起的变化。
在对照组和脑积水诱导组的标本中,未观察到反映GER的食管和胃改变的组织学证据。与对照组相比,脑积水组食管和胃底平滑肌对氯化钾和毒蕈碱受体激动剂卡巴胆碱的最大收缩反应增强。这些变化具有统计学意义。两组脑积水组食管肌条对β肾上腺素能受体激动剂异丙肾上腺素的舒张反应相似。然而,与对照组相比,脑积水诱导组胃底肌条对异丙肾上腺素的舒张反应明显降低。两组食管和胃底平滑肌条对罂粟碱的舒张反应相似。
我们的研究揭示了脑积水诱导的幼鼠前肠平滑肌反应性在受体依赖性和非依赖性方面的改变。因此,我们认为平滑肌反应性受损至少部分可能导致脑积水患者出现前肠运动功能异常。