Ye-Cheng Liu1, Zhi-Wei Qi1, Shi-Gong Guo1, Zhong Wang1, Xue-Zhong Yu1, Sui Ma1. 1. Emergency Medicine Department, Peking Union Medical College Hospital, Beijing 100730, China (Liu YC, Wang Z, Yu XZ, Ma S); China-Japan Friendship Hospital, Beijing 100029, China (Qi ZW); Weston General Hospital, UK (Guo SG).
Abstract
BACKGROUND: Corticotrophin releasing hormone (CRH) is believed to mediate stress-induced behaviors, implying a broader, integrative role for the hormone in the psychological stress response, and studies on CRH in physical stress are few. This study was undertaken to investigate whether CRH plays an important role in cerebral infarction-related gastrointestinal barrier dysfunction. METHODS: Thirty male Wistar rats were randomly divided into a pseudo-operation group (group C, n=10), a cerebral infarction group (group I, n=10), and a cerebral infarction + ic α-helical-CRH (9-41) group (group Aic, n=10). Urine samples were collected to determine the levels of epinephrine, norepinephrine, cortisol, and sucrose. At 24 hours after establishment of the models, blood samples were taken to determine the activity of diamine oxidase (DAO) and the concentration of D-lactic acid (D-lac). The stomach was taken to determine gastric Guth score, and the hypothalamus was also taken to determine tissue CRH protein expression using Western blotting. RESULTS: The hypothalamus CRH protein, the indicators of stress, the plasma DAO activity and plasma D-lac, urine sucrose exertion and gastric Guth score in group I were higher than those in groups Aic and C. CONCLUSIONS: After cerebral infarction, CRH in the hypothalamus was increased, the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system were activated, gastrointestinal permeability was increased, and gastrointestinal barrier function was destroyed. CRH receptor antagonist alleviated the gastrointestinal barrier function.
BACKGROUND:Corticotrophin releasing hormone (CRH) is believed to mediate stress-induced behaviors, implying a broader, integrative role for the hormone in the psychological stress response, and studies on CRH in physical stress are few. This study was undertaken to investigate whether CRH plays an important role in cerebral infarction-related gastrointestinal barrier dysfunction. METHODS: Thirty male Wistar rats were randomly divided into a pseudo-operation group (group C, n=10), a cerebral infarction group (group I, n=10), and a cerebral infarction + ic α-helical-CRH (9-41) group (group Aic, n=10). Urine samples were collected to determine the levels of epinephrine, norepinephrine, cortisol, and sucrose. At 24 hours after establishment of the models, blood samples were taken to determine the activity of diamine oxidase (DAO) and the concentration of D-lactic acid (D-lac). The stomach was taken to determine gastric Guth score, and the hypothalamus was also taken to determine tissue CRH protein expression using Western blotting. RESULTS: The hypothalamusCRH protein, the indicators of stress, the plasma DAO activity and plasma D-lac, urine sucrose exertion and gastric Guth score in group I were higher than those in groups Aic and C. CONCLUSIONS: After cerebral infarction, CRH in the hypothalamus was increased, the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system were activated, gastrointestinal permeability was increased, and gastrointestinal barrier function was destroyed. CRH receptor antagonist alleviated the gastrointestinal barrier function.
Authors: K B Mackay; H Bozigian; D E Grigoriadis; S A Loddick; G Verge; A C Foster Journal: J Cereb Blood Flow Metab Date: 2001-10 Impact factor: 6.200