Taché Y, Mönnikes H, Bonaz B, Rivier J
CURE/Digestive Disease Center, V.A. Wadsworth Medical Center, Los Angeles, California 90073.
Ann N Y Acad Sci. 1993 Oct 29;697:233-43. doi: 10.1111/j.1749-6632.1993.tb49936.x.
Major advances have been made in the understanding of the pathophysiology of stress-related alteration of gut function. A wealth of information indicates that CRF is involved in the central mechanisms by which stress inhibits gastric emptying while stimulating colonic motor function. CRF acts in the PVN to trigger both the inhibition of gastric emptying and the stimulation of colonic motor function in response to stress, in addition to previously established endocrine and behavioral responses. Preliminary evidence exists that CRF acts in the locus coeruleus to induce a selective stimulation of colonic transit without influencing gastric emptying. The central actions of CRF to alter gastric and colonic motor function are conveyed by autonomic pathways and are unrelated to the associated stimulation of pituitary hormone secretion. The demonstration that central CRF plays a role in mediating gastric stasis resulting from surgery, peritonitis or high levels of central interleukin-1 provides new insight into the mechanisms involved in gastric ileus induced postoperatively or by infectious disease. Likewise, the demonstration that CRF in the PVN and locus coeruleus induce the anxiogenic and colonic motor responses to stress and that colonic distention activates neurons in the locus coeruleus opens new avenues for the understanding of the pathogenesis of a subset of IBS patients with colonic hypersensitivity associated with psychopathological disturbance and diarrhea-predominant symptoms.
在应激相关肠道功能改变的病理生理学理解方面已取得重大进展。大量信息表明，促肾上腺皮质激素释放因子（CRF）参与了应激抑制胃排空同时刺激结肠运动功能的中枢机制。除了先前已确定的内分泌和行为反应外，CRF在室旁核（PVN）发挥作用，以触发对应激的胃排空抑制和结肠运动功能刺激。有初步证据表明，CRF在蓝斑核发挥作用，诱导结肠转运的选择性刺激而不影响胃排空。CRF改变胃和结肠运动功能的中枢作用通过自主神经通路传递，且与垂体激素分泌的相关刺激无关。中枢CRF在介导手术、腹膜炎或中枢白细胞介素-1高水平导致的胃淤滞中起作用，这一发现为术后或传染病引起的胃麻痹所涉及的机制提供了新的见解。同样，室旁核和蓝斑核中的CRF诱导对应激的焦虑和结肠运动反应，以及结肠扩张激活蓝斑核中的神经元，这一发现为理解一部分伴有精神病理障碍和腹泻为主症状的结肠高敏性肠易激综合征（IBS）患者的发病机制开辟了新途径。
