1. Leucocyte and platelet adhesion in different layers of the small bowel during experimental total warm ischaemia and reperfusion.
- Author
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Beuk RJ, Tangelder GJ, Maassen RL, Quaedackers JS, Heineman E, and Oude Egbrink MG
- Subjects
- Animals, Antibodies, Monoclonal pharmacology, Blood Flow Velocity physiology, Capillaries physiology, Cell Adhesion physiology, Intercellular Adhesion Molecule-1 immunology, Microcirculation physiology, Platelet Activating Factor antagonists & inhibitors, Platelet Aggregation Inhibitors pharmacology, Pyridinium Compounds pharmacology, Random Allocation, Rats, Rats, Inbred Lew, Reperfusion methods, Reperfusion Injury immunology, Tetrahydroisoquinolines pharmacology, Warm Ischemia methods, Intercellular Adhesion Molecule-1 physiology, Intestine, Small blood supply, Leukocytes physiology, Platelet Activating Factor physiology, Platelet Adhesiveness physiology
- Abstract
Background: Ischaemia and reperfusion (IR) of the small bowel is involved in many clinical conditions. A key component in IR-induced tissue damage is microvascular dysfunction. The aim was to investigate the role of leucocytes and platelets in capillary flow impediment and tissue damage., Methods: Anaesthetized rats were subjected to 30 min warm ischaemia of the small bowel, followed by 1 h reperfusion. To elucidate the influence of leucocytes on platelet adhesion, leucocyte-vessel wall interactions induced by IR were prevented by anti-platelet activating factor (PAF) or anti-intercellular adhesion molecule (ICAM)-1. Intravital videomicroscopy was performed and tissue injury was evaluated histologically., Results: In submucosal venules, IR induced an increase in the median number of interacting leucocytes from 3 to 10 and 20 leucocytes per 100-microm venule segment after 10 and 60 min reperfusion respectively. Anti-PAF or anti-ICAM-1 completely attenuated this increase, resulting in an eightfold improvement in submucosal capillary flow and reduced tissue injury. Shedding of villi no longer occurred. Platelet-vessel wall interactions occurred particularly in submucosal venules, but were not affected by anti-PAF or anti-ICAM-1., Conclusion: Small bowel IR initiated an inflammatory and thrombotic response in the submucosal layer only. Attenuation of leucocyte adhesion improved submucosal capillary perfusion, preventing shedding of mucosal villi.
- Published
- 2008
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