Effects of different durations of total warm ischemia of the gut on rat mesenteric microcirculation.

BACKGROUND: Gut injury due to ischemia and reperfusion (I/R) plays a pivotal role in many clinical conditions, such as small bowel transplantation, heart or aortic surgery in adults, and necrotizing enterocolitis in neonates. The influence of ischemic events on microcirculatory mechanisms is not well understood. Therefore, we studied, in vivo, local perfusion and leukocyte-vessel wall interactions before and after different periods of total warm ischemia of the whole gut and subsequent reperfusion in mesenteric microvessels. MATERIALS AND METHODS: Groups of pentobarbital-anaesthetized Lewis rats were subjected to 15 (n = 9), 30 (n = 12), or 60 min (n = 5) of total warm gut ischemia and 2 h reperfusion. As control a sham group (n = 10) was included. After ligating the inferior mesenteric artery, total warm ischemia was induced by clamping the superior mesenteric artery. Before and at different time periods after start of reperfusion intravital video microscopic measurements were performed. RESULTS: Rats subjected to 60 min ischemia died during the early reperfusion phase. Fifteen, 30, and 60 min ischemia induced in venules a significant decrease in blood flow, while diameter changes were not observed. This flow decrease was severe in the 15- and 30-min ischemia groups, dropping to 40 and 25% of control, respectively. Following 60 min ischemia blood flow did not exceed 10% of control. The total number of interacting leukocytes, a parameter which includes both leukocyte rolling and adhesion in venules, increased up to 5 or 10 times its control value following 15 or 30 min ischemia, respectively. Leukocyte-vessel wall interactions could not be studied in the 60-min ischemia group, due to the low blood flow. CONCLUSIONS: Even short periods of total warm ischemia of the whole gut induce severe attenuation of venular blood flow with an increase in leukocyte-vessel wall interactions. These changes increase with prolongation of the ischemic period. A 60-min period of total warm ischemia is fatal during the early reperfusion phase.

Ischemia/reperfusion injury in rat mesenteric venules: red blood cell velocity and leukocyte rolling.

The authors determined the effects of 15 (n = 9) and 30 (n = 12) minutes of warm ischemia on the rat mesentery and compared the results with those of a sham-operated group (n = 10). Red blood cell velocity and number of rolling leukocytes were assessed before ischemia as well as 10, 20, 30, 60, 90, and 120 minutes after the start of reperfusion. Leukocyte rolling is considered to be an early step of the inflammatory process. Leukocytes roll along the vessel wall at a velocity that is clearly lower than that of the other blood cells. The preischemic values of red blood cell velocity and number of rolling leukocytes in the 15- and 30-minute ischemia groups did not differ from those of the sham group. In the sham group, no significant changes in red blood cell velocity and number of rolling leukocytes were observed over time. Compared with the sham group, the red blood cell velocity of the 15-minute ischemia group was significantly lower at 30, 60, 90, and 120 minutes after the start of reperfusion the number of rolling leukocytes did not differ significantly. For the 30-minute ischemia group, red blood cell velocity also was significantly lower at 20, 30, 60, 90, and 120 minutes after the start of reperfusion, and the number of rolling leukocytes was higher at 10, 20, and 30 minutes after the start of reperfusion. The results of this study indicate that short periods of total warm ischemia of the rat small bowel and subsequent reperfusion result in a significantly impaired microcirculatory blood flow in the mesentery. However, a prolonged period of ischemia is required to increase leukocyte-vessel wall interactions. In the future, this model will enable us to study the effect of pharmacological interventions during an early stage of the inflammatory response to ischemia/reperfusion in the gut.