AIM: To investigate whether peripheral corticotropin releasing hormone (CRH), which is up-regulated in intestinal inflammation, mediates the post-inflammatory visceral hypersensitivity in a rat model of colitis. METHODS: We measured mucosal myeloperoxidase (MPO) activity as a marker of inflammation, plasma CRH level, and abdominal withdrawal reflex (AWR) to colorectal distension as a visceral nociceptive response at 2, 7 and 14 d after the induction of colitis with 4% acetic acid. RESULTS: Colonic inflammation, quantified by MPO activity, significantly increased on d 2 and subsided thereafter, which indicated a resolution of inflammation within 7 d. On the contrary, plasma CRH level and AWR score were increased on d 2, remained high on d 7, and returned to control level on d 14. Intraperitoneal injection of a CRH antagonist, astressin (30 mug/kg), significantly attenuated the post-inflammatory visceral hypersensitivity on d 7. Furthermore, intraperitoneal administration of CRH (3 and 10 mug/kg) mimicked the post-inflammatory visceral hypersensitivity in naive rats. CONCLUSION: These results suggest that increased peripheral CRH mediates the enhanced visceral nociception in rats recovered from experimental colitis.
AIM: To investigate whether peripheral corticotropin releasing hormone (CRH), which is up-regulated in intestinal inflammation, mediates the post-inflammatory visceral hypersensitivity in a rat model of colitis. METHODS: We measured mucosal myeloperoxidase (MPO) activity as a marker of inflammation, plasma CRH level, and abdominal withdrawal reflex (AWR) to colorectal distension as a visceral nociceptive response at 2, 7 and 14 d after the induction of colitis with 4% acetic acid. RESULTS:Colonic inflammation, quantified by MPO activity, significantly increased on d 2 and subsided thereafter, which indicated a resolution of inflammation within 7 d. On the contrary, plasma CRH level and AWR score were increased on d 2, remained high on d 7, and returned to control level on d 14. Intraperitoneal injection of a CRH antagonist, astressin (30 mug/kg), significantly attenuated the post-inflammatory visceral hypersensitivity on d 7. Furthermore, intraperitoneal administration of CRH (3 and 10 mug/kg) mimicked the post-inflammatory visceral hypersensitivity in naive rats. CONCLUSION: These results suggest that increased peripheral CRH mediates the enhanced visceral nociception in rats recovered from experimental colitis.
Authors: Ines Schwetz; James A McRoberts; Santosh V Coutinho; Sylvie Bradesi; Greg Gale; Michael Fanselow; Mulugeta Million; Gordon Ohning; Yvette Taché; Paul M Plotsky; Emeran A Mayer Journal: Am J Physiol Gastrointest Liver Physiol Date: 2005-06-30 Impact factor: 4.052
Authors: P G McLean; C Picard; R Garcia-Villar; R Ducos de Lahitte; J Moré; J Fioramonti; L Buéno Journal: Neurogastroenterol Motil Date: 1998-12 Impact factor: 3.598
Authors: E A Linton; A V Perkins; P Hagan; S Poole; A F Bristow; F Tilders; R Corder; C D Wolfe Journal: J Endocrinol Date: 1995-07 Impact factor: 4.286
Authors: Fatemeh Dolatabadi; Amir H Abdolghaffari; Mohammad H Farzaei; Maryam Baeeri; Fatemeh S Ziarani; Majid Eslami; Mohammad Abdollahi; Roja Rahimi Journal: J Neurogastroenterol Motil Date: 2018-07-30 Impact factor: 4.924