Effect of somatostatin on gastrointestinal contractility in Schistosoma mansoni infected mice

Effect of somatostatin on gastrointestinal contractility in Schistosoma mansoni infected mice
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DOI:
10.1016/s0020-7519(02)00128-5
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发表时间:
2002-09-01
影响因子:
4
通讯作者:
Pelckmans, PA
Pelckmans, PA
中科院分区:
医学2区
文献类型:
--
作者:
De Man, JG;Chatterjee, S;Pelckmans, PA

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曼氏血吸虫感染会引起严重的胃肠动力障碍,其特征是肠肌过度活跃、腹痛、腹泻、呕吐和恶心。在血吸虫病期间,神经肽生长抑素在炎性肉芽肿内产生。然而,生长抑素也是胃肠动力的重要抑制调节剂。在本研究中,我们研究了生长抑素减少血吸虫病引起的胃肠平滑肌过度活跃的潜力。进行器官浴实验以研究来自对照小鼠和感染曼氏链球菌2、4、8和16周的小鼠的分离的肠道平滑肌条的收缩性。肠神经的电场刺激(0.5-8 Hz)诱导小肠所有区域中胆碱能起源的频率依赖性神经源性收缩。生长抑素 (0.1-1 muM) 浓度依赖性地抑制未感染对照小鼠和曼氏沙门氏菌急性感染小鼠(感染 2 周和 4 周)小肠中肠神经刺激的收缩。曼氏链球菌感染8周后,生长抑素的这种抑制作用不太明显,感染16周后完全消失。组织学表明,小鼠慢性感染曼氏沙门氏菌与小肠肌肉组织的显着改变有关。这些改变可能与生长抑素反应性的生理变化有关,并表明在慢性曼氏血吸虫病期间,小肠中肠道神经传递的生长抑素神经调节回路受到干扰。 (C) 2002 年澳大利亚寄生虫学协会。由 Elsevier Science Ltd 出版。保留所有权利。
Schistosoma mansoni infection induces severe gastrointestinal motility disturbances which are characterised by hyperactivity of intestinal muscle, abdominal pain, diarrhoea, vomiting and nausea. During schistosomiasis, the neuropeptide somatostatin is generated within inflammatory granulomas. However, somatostatin is also an important inhibitory modulator of gastrointestinal motility. In the present study, we have investigated the potential of somatostatin to reduce schistosomiasis-induced hyperactivity of gastrointestinal smooth muscle. Organ bath experiments were performed to study the contractility of isolated smooth muscle strips of intestine from control mice and from mice that were infected with S. mansoni for 2, 4, 8 and 16 weeks. Electrical field stimulation (0.5-8 Hz) of enteric nerves induced frequency-dependent neurogenic contractions of cholinergic origin in all regions of the small intestine. Somatostatin (0.1-1 muM) concentration-dependently inhibited the contractions to enteric nerve stimulation in the small intestine from uninfected control mice and from acutely S. mansoni infected mice (2 and 4 weeks of infection). After 8 weeks of infection with S. mansoni, this inhibitory effect of somatostatin was less pronounced and after 16 weeks of infection it was completely abolished. Histology demonstrated that chronic infection of mice with S. mansoni was associated with significant alterations in the musculature of the small intestine. These alterations may be associated with physiological changes in the responsiveness to somatostatin and suggest that the somatostatin neuroregulatory circuit of enteric neurotransmission in the small intestine is disturbed during chronic schistosomiasis mansoni. (C) 2002 Australian Society for Parasitology Inc. Published by Elsevier Science Ltd. All rights reserved.