M Boros1, J Kaszaki, B Ordögh, S Nagy. 1. Institute of Experimental Surgery and Department of Otorhinolaryngology, Szent-Györgyi Albert Medical University, Szeged, Hungary. boros@expsur.szote.u-szeged.hu
Abstract
OBJECTIVE: To determine the impact of previous mast cell degranulation on intestinal ischemia-reperfusion-induced mucosal damaged. MATERIALS: The hemodynamic and morphological consequences of complete arterial occlusion were evaluated in anesthetized dogs. The mast cell degranulator Cremophor-E1 (n = 5) and Compound 48/80 (n = 5) were used to investigate the involvement of gastrointestinal mast cells in ischemia-reperfusion-induced tissue reactions. Seven dogs subjected to complete segmental arterial occlusion served as controls. Intestinal biopsies taken at the end of 120-min ischemia and after 120 min of reperfusion were evaluated histologically. METHODS: The number of mast cells was determined and the degree of mucosal damage was evaluated according to the 5 grade Chiu scale. Mucosal histidine decarboxylase activity was measured in tissue samples and the rate of release of histamine was determined from the venous effluent of the ileal segment. RESULTS: In the control group, 120-min reperfusion significantly increased the plasma histamine level, and induced a severe tissue injury. In the compound 48/80 and Cremophor-E1-pretreated groups, the reduction in the baseline number of mast cells in the villi was 37% and 53%, respectively, and the ischemia-reperfusion-induced release of histamine was significantly decreased. In these groups, the basal mucosal histidine decarboxylase activity was significantly increased and the degree of damage of the intestinal mucosa was significantly reduced. CONCLUSION: It is proposed that mast cell degranulation prior to ischemia may induce a potentially protective mechanism in the small bowel mucosa and decreases ischemia-reperfusion injury in the dog.
OBJECTIVE: To determine the impact of previous mast cell degranulation on intestinal ischemia-reperfusion-induced mucosal damaged. MATERIALS: The hemodynamic and morphological consequences of complete arterial occlusion were evaluated in anesthetized dogs. The mast cell degranulator Cremophor-E1 (n = 5) and Compound 48/80 (n = 5) were used to investigate the involvement of gastrointestinal mast cells in ischemia-reperfusion-induced tissue reactions. Seven dogs subjected to complete segmental arterial occlusion served as controls. Intestinal biopsies taken at the end of 120-min ischemia and after 120 min of reperfusion were evaluated histologically. METHODS: The number of mast cells was determined and the degree of mucosal damage was evaluated according to the 5 grade Chiu scale. Mucosal histidine decarboxylase activity was measured in tissue samples and the rate of release of histamine was determined from the venous effluent of the ileal segment. RESULTS: In the control group, 120-min reperfusion significantly increased the plasma histamine level, and induced a severe tissue injury. In the compound 48/80 and Cremophor-E1-pretreated groups, the reduction in the baseline number of mast cells in the villi was 37% and 53%, respectively, and the ischemia-reperfusion-induced release of histamine was significantly decreased. In these groups, the basal mucosal histidine decarboxylase activity was significantly increased and the degree of damage of the intestinal mucosa was significantly reduced. CONCLUSION: It is proposed that mast cell degranulation prior to ischemia may induce a potentially protective mechanism in the small bowel mucosa and decreases ischemia-reperfusion injury in the dog.