BACKGROUND & AIMS: Induction of heat-shock protein 72 is associated with enhanced tolerance to subsequent nonthermal stresses. This study evaluated whether induction of heat-shock protein 72 protects against intestinal ischemia/reperfusion injury. METHODS: Groups of nonheated and heated rats underwent sham operation, 30 minutes of ischemia by occlusion of the superior mesenteric artery, or ischemia followed by 60 minutes of reperfusion. Whole-body hyperthermia to a core temperature of 41.5-42 degrees C for 15-20 minutes was followed by passive cooling 2-3 hours before the experiment. Samples of small intestine were obtained for determination of heat-shock protein 72 production and ex vivo generation of prostaglandin E2 and leukotriene B4 and for histological assessment of mucosal injury and number of neutrophils. RESULTS: Hyperthermia significantly increased heat-shock protein 72 production and significantly reduced ischemia/reperfusion-induced mucosal injury, neutrophilic infiltration, and leukotriene B4 production. Levels of leukotriene B4 and numbers of neutrophils were well correlated in nonheated (r = 0.72) but not in heated groups (r = -0.16). The elevation of prostaglandin E2 levels in response to ischemia and reperfusion was unaltered by hyperthermia. CONCLUSIONS: The mechanism of heat stress-induced protection against intestinal ischemia/reperfusion injury involves inhibition of leukotriene B4 production and subsequent prevention of neutrophil activation and chemotaxis.
BACKGROUND & AIMS: Induction of heat-shock protein 72 is associated with enhanced tolerance to subsequent nonthermal stresses. This study evaluated whether induction of heat-shock protein 72 protects against intestinal ischemia/reperfusion injury. METHODS: Groups of nonheated and heated rats underwent sham operation, 30 minutes of ischemia by occlusion of the superior mesenteric artery, or ischemia followed by 60 minutes of reperfusion. Whole-body hyperthermia to a core temperature of 41.5-42 degrees C for 15-20 minutes was followed by passive cooling 2-3 hours before the experiment. Samples of small intestine were obtained for determination of heat-shock protein 72 production and ex vivo generation of prostaglandin E2 and leukotriene B4 and for histological assessment of mucosal injury and number of neutrophils. RESULTS:Hyperthermia significantly increased heat-shock protein 72 production and significantly reduced ischemia/reperfusion-induced mucosal injury, neutrophilic infiltration, and leukotriene B4 production. Levels of leukotriene B4 and numbers of neutrophils were well correlated in nonheated (r = 0.72) but not in heated groups (r = -0.16). The elevation of prostaglandin E2 levels in response to ischemia and reperfusion was unaltered by hyperthermia. CONCLUSIONS: The mechanism of heat stress-induced protection against intestinal ischemia/reperfusion injury involves inhibition of leukotriene B4 production and subsequent prevention of neutrophil activation and chemotaxis.
Authors: M Jin; M Otaka; S Otani; A Okuyama; S Itoh; A Iwabuchi; H Sasahara; S Fujimori; H Itoh; Y Tashima; O Masamune Journal: J Gastroenterol Date: 1997-02 Impact factor: 7.527
Authors: K Horst; F Hildebrand; R Pfeifer; S Hübenthal; K Almahmoud; M Sassen; T Steinfeldt; H Wulf; S Ruchholtz; H C Pape; D Eschbach Journal: Eur J Trauma Emerg Surg Date: 2015-02-28 Impact factor: 3.693
Authors: Eliseu O De Oliveira; Kan Wang; Hye-Sik Kong; Suhyon Kim; Matthew Miessau; Robert J Snelgrove; Y Michael Shim; Mikell Paige Journal: Bioorg Med Chem Lett Date: 2011-09-20 Impact factor: 2.823