Total warm ischemia and reperfusion impairs flow in all rat gut layers butincreases leukocyte-vessel wall interactions in the submucosa only

Objective To study the effect of warm ischemia and reperfusion (I/R) on local perfusi on and leukocyte-vessel wall interactions in vivo in all small bowel layers , and to quantify small bowel tissue injury histologically and by measuring intestinal fatty acid binding protein (I-FABP) release from the enterocyte s. Summary Background Data Gut injury as a result of I/R plays a pivotal role in a variety of clinical conditions, such as small bowel transplantation, heart or aortic surgery, and (septic) shock. The precise mechanism behind I/R injury and the role of microvascular changes remain unclear. The influence of warm I/R of the gut on microvascular parameters in the different gut layers has not been studi ed before. Methods Anesthetized Lewis rats were either subjected to 30 minutes of ischemia and 1 hour of reperfusion or sham-treated as controls, After ligating the infe rior mesenteric artery, total warm ischemia was induced by clamping the sup erior mesenteric artery. Intravital video microscopic measurements were obt ained at intervals. Tissue injury of the small bowel and other organs was h istologically evaluated afterward. In addition, plasma levels of I-FABP wer e determined to measure enterocyte damage. Results After ischemia, mean red blood cell velocity decreased significantly in all layers of the small bowel, but no diameter changes were observed. Leukocyt e-vessel wall interactions increased in the submucosa but not in the muscle layers. Plasma levels of I-FABP significantly increased from 30 minutes of reperfusion onward. The intestinal mucosa was severely injured; no histolo gic damage was detected in other tissues. Conclusions This is the first in vivo study showing that total warm ischemia of the rat gut impairs perfusion in the whole small bower, whereas leukocyte-vessel w all interactions increase in the submucosal layer only. Therefore, the earl y inflammatory response to I/R seems to be limited to the submucosa. Both m icrovascular effects may have contributed to the severe morphologic and fun ctional mucosal injury observed after I/R.