Role of Stress in Functional Gastrointestinal Disorders

Role of Stress in Functional Gastrointestinal Disorders
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压力在功能性胃肠道疾病中的作用

DOI:
--
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发表时间:
2001
期刊:
影响因子:
2.3
通讯作者:
I. Heymann
I. Heymann
中科院分区:
医学3区
文献类型:
--
作者:
Hubert Mönnikes;J. J. Tebbe;M. Hildebrandt;Petra C. Arck;E. Osmanoglou;Matthias Rose;B. Klapp;B. Wiedenmann;I. Heymann

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心理应激被广泛认为在功能性胃肠道(GI)疾病,特别是肠易激综合征(IBS)中起主要作用,通过加速症状的恶化。现有数据清楚地表明,抑制胃排空和刺激结肠运输是胃肠道对急性或短期应激的动力反应中最一致的模式。因此,人们可能会提出,这些变化可能发挥消化不良症状和改变,在大便频率和一致性与应激相关的功能性胃肠道疾病的患者的病理生理作用。综上所述,上述研究表明IBS患者结肠运动对应激的反应被夸大。有证据表明,增加的情绪反应与结肠的这种差异有关,也许还有胃对某些应激源的运动反应。然而,几乎没有有效的数据,迄今为止,从人类研究解决的问题,如果运动性反应的差异与功能性胃肠道疾病患者和健康受试者之间的压力是由于改变与自主神经系统的不平衡或增加应激敏感性相关的应激反应。我们可以总结,在实验动物中,各种心理和生理应激源诱导的胃肠道运动改变的最一致模式是延迟胃排空和加速结肠运输。脑内内源性促肾上腺皮质激素释放因子(CRF)通过激活脑内CRF受体在中枢神经系统介导应激引起的上消化道抑制和下消化道运动功能刺激中起重要作用。CRF对胃排空的抑制作用可能是通过与CRF-2受体的相互作用来介导的,而CRF-1受体则参与结肠和焦虑对应激的反应。内源性5-羟色胺,外周释放的压力,似乎参与了压力和中央CRF诱导的刺激结肠动力作用于5 HT-3受体。总之,从健康受试者和功能性胃肠道疾病患者的研究中获得的有限数据提供了一些证据,表明应激会影响人类的内脏敏感性。急性心理应激似乎有利于增加敏感性的实验内脏刺激,如果应激源引起了显着的情绪变化。总之,在实验动物中的研究表明,应激诱导的内脏高敏感性是由内源性CRF和情绪运动系统的结构(例如杏仁核)的参与中枢介导的。应激诱导的胃肠道粘膜肥大细胞的活化或致敏似乎参与了应激相关的内脏敏感性改变。
Psychological stress is widely believed to play a major role in functional gastrointestinal (GI) disorders, especially irritable bowel syndrome (IBS), by precipitating exacerbation of symptoms. The available data clearly demonstrate that inhibition of gastric emptying and stimulation of colonic transit is the most consistent pattern in the motility response of the GI tract to acute or short-term stress. Thus, one might propose that these alterations might play a pathophysiological role in dyspeptic symptoms and alterations in stool frequency and consistency in patients with stress-related functional GI disorders. Taken together, the above-mentioned studies suggest that the colonic motor response to stress is exaggerated in IBS. There is evidence that an increased emotional response is associated with this difference in colonic, and perhaps also gastric motor responses to certain stressors. However, almost no valid data are available so far from human studies addressing the question if differences in motility responses to stress between patients with functional GI disorders and healthy subjects are due to an altered stress response associated with an imbalance of the autonomic nervous system or increased stress susceptibility. We can summarize that in experimental animals the most consistent pattern of GI motor alterations induced by various psychological and physical stressors is that of delaying gastric emptying and accelerating colonic transit. Endogenous corticotropin-releasing factor (CRF) in the brain plays a significant role in the central nervous system mediation of stress-induced inhibition of upper GI and stimulation of lower GI motor function through activation of brain CRF receptors. The inhibition of gastric emptying by CRF may be mediated by interaction with the CRF-2 receptor, while CRF-1 receptors are involved in the colonic and anxiogenic responses to stress. Endogenous serotonin, peripherally released in response to stress, seems to be involved in stress- and central CRF-induced stimulation of colonic motility by acting on 5HT-3 receptors. Taken together, the limited data available from investigations in healthy subjects and patients with functional GI disorders provide some evidence that stress affects visceral sensitivity in humans. Acute psychological stress seems to facilitate increased sensitivity to experimental visceral stimuli, if the stressor induces a significant emotional change. In summary, studies in experimental animals suggest that stress-induced visceral hypersensitivity is centrally mediated by endogenous CRF and involvement of structures of the emotional motor system, e.g. the amygdala. Stress-induced activation or sensitization of mucosal mast cells in the GI tract seem to be involved in stress-associated alterations of visceral sensitivity.
通过中枢神经系统扰乱胃排空和十二指肠运动。
DOI: --
发表时间: 1982
期刊: Gastroenterology
影响因子: 29.4
作者:
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通讯作者: Malagelada,JR
DOI: 10.1016/0016-5085(90)90332-u
发表时间: 1990-05-01
期刊: GASTROENTEROLOGY
影响因子: 29.4
作者:
WHITEHEAD, WE;HOLTKOTTER, B;SCHUSTER, MM
通讯作者: SCHUSTER, MM
DOI: 10.1016/0016-5085(93)91006-4
发表时间: 1993-03
期刊: Gastroenterology
影响因子: 29.4
作者:
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通讯作者: H. Mönnikes;B. Schmidt;Y. Taché
DOI: 10.1152/ajpgi.2001.280.2.g173
发表时间: 2001-02-01
影响因子: 4.5
作者:
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通讯作者: Wang, LX
DOI: 10.1152/ajpgi.1998.274.6.g1094
发表时间: 1998-06-01
影响因子: 4.5
作者:
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