Ischemia-reperfusion protects the rat small intestine against subsequent injury

Citation
Tj. Miner et al., Ischemia-reperfusion protects the rat small intestine against subsequent injury, J SURG RES, 82(1), 1999, pp. 1-10
Citations number
41
Categorie Soggetti
Surgery,"Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF SURGICAL RESEARCH
ISSN journal
00224804 → ACNP
Volume
82
Issue
1
Year of publication
1999
Pages
1 - 10
Database
ISI
SICI code
0022-4804(199903)82:1<1:IPTRSI>2.0.ZU;2-H
Abstract
Background. It has been suggested that multiple sublethal insults are commo nly associated with the development of multiple organ failure (MOF). The gu t is considered to be pivotal in the pathogenesis of MOF. This study invest igated the effects of repeated ischemia-reperfusion of the rat small intest ine. Methods. Groups of rats underwent 30 min of superior mesenteric artery occl usion or sham operation followed by 24 h of reperfusion. They then received an additional 30 min of superior mesenteric artery occlusion and 2 h of re perfusion or sham operation. Small intestine was examined for mucosal injur y, neutrophil infiltration, goblet cell number, and generation of the eicos anoids, prostaglandin E-2, and leukotriene B-4. Activation of neutrophils w as assessed in systemic venous blood. Results, Animals subjected to two insults of ischemia-reperfusion demonstra ted significantly less mucosal injury than animals undergoing one episode o f ischemia and 2 h of reperfusion, despite increased neutrophil infiltratio n, leukotriene B-4, and activated systemic neutrophils. Goblet cell number was elevated in animals 24 h after the fist ischemia-reperfusion insult and remained enhanced after the second episode of ischemia-reperfusion. Conclusions. The initial episode of ischemia-reperfusion caused an adaptive response associated with cytoarchitectural preservation following the subs equent insult. Increased mucus production was associated with mucosal prote ction. Nevertheless, repeated ischemia-reperfusion potentiated the local in flammatory response and the systemic activation of neutrophils.