Beuk R J, Heineman E, Tangelder G J, Kurvers H A, Bonke H J, oude Egbrink M G
Cardiovascular Research Institute Maastricht (CARIM), University Hospital Maastricht, Maastricht, The Netherlands.
J Surg Res. 1997 Nov;73(1):14-23. doi: 10.1006/jsre.1997.5204.
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.
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.
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.
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.
缺血再灌注(I/R)所致的肠道损伤在许多临床病症中起关键作用,如小肠移植、成人心脏或主动脉手术以及新生儿坏死性小肠结肠炎。缺血事件对微循环机制的影响尚未完全明确。因此,我们在体内研究了全肠道不同时长的完全热缺血及随后肠系膜微血管再灌注前后的局部灌注及白细胞与血管壁的相互作用。
将戊巴比妥麻醉的Lewis大鼠分组,分别进行15分钟(n = 9)、30分钟(n = 12)或60分钟(n = 5)的全肠道热缺血及2小时再灌注。设假手术组(n = 10)作为对照。结扎肠系膜下动脉后,通过夹闭肠系膜上动脉诱导完全热缺血。在再灌注开始前及不同时间段进行活体视频显微镜测量。
经历60分钟缺血的大鼠在再灌注早期死亡。15分钟、30分钟和60分钟的缺血均导致小静脉血流显著减少,而未观察到直径变化。15分钟和30分钟缺血组的血流减少严重,分别降至对照值的40%和25%。60分钟缺血后血流未超过对照值的10%。相互作用的白细胞总数(一个包括白细胞在小静脉内滚动和黏附的参数)在15分钟或30分钟缺血后分别增加至对照值的5倍或10倍。由于血流过低,60分钟缺血组无法研究白细胞与血管壁的相互作用。
即使是全肠道短时间的完全热缺血也会导致小静脉血流严重减少,并伴有白细胞与血管壁相互作用增加。这些变化随缺血时间延长而加剧。60分钟的全肠道热缺血在再灌注早期是致命的。