Abstract | BACKGROUND & AIMS: 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: 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.
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Authors | A Stojadinovic, J Kiang, R Smallridge, R Galloway, T Shea-Donohue |
Journal | Gastroenterology
(Gastroenterology)
Vol. 109
Issue 2
Pg. 505-15
(Aug 1995)
ISSN: 0016-5085 [Print] United States |
PMID | 7615200
(Publication Type: Journal Article)
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Chemical References |
- HSP72 Heat-Shock Proteins
- Heat-Shock Proteins
- Leukotriene B4
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Topics |
- Animals
- Blood Pressure
(physiology)
- Fever
- HSP72 Heat-Shock Proteins
- Heart Rate
(physiology)
- Heat-Shock Proteins
(biosynthesis)
- Intestinal Mucosa
(blood supply, metabolism, pathology)
- Intestine, Small
(blood supply, metabolism, pathology)
- Leukotriene B4
(biosynthesis)
- Male
- Neutrophils
(physiology)
- Rats
- Rats, Sprague-Dawley
- Reperfusion Injury
(metabolism, pathology, prevention & control)
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