Nezu Yoshinori, Tagawa Masahiro, Sakaue Yoko, Hara Yasushi, Tsuchida Shuichi, Ogawa Ryo
Department of Veterinary Science, Division of Veterinary Surgery, Nippon Veterinary and Animal Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo 18048602, Japan.
Am J Vet Res. 2002 Dec;63(12):1680-6. doi: 10.2460/ajvr.2002.63.1680.
To determine whether small intestinal ischemia and reperfusion induces bacterial translocation and proinflammatory cytokine response in either the systemic or portal circulation in dogs.
17 healthy adult Beagles.
The superior mesenteric artery (SMA) was occluded for 0 (group-3 dogs), 30 (group-1 dogs), or 60 (group-2 dogs) minutes, followed by reperfusion for 180 minutes; serum lactate and endotoxin concentrations and tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 activities in the systemic and portal circulation and intramucosal pH were measured at various time points.
In group-2 dogs, TNFalpha activity was found to be significantly increased in the portal circulation, peaking at 60 minutes of reperfusion; TNF-alpha activity, in the systemic circulation, gradually increased from 60 minutes of reperfusion to the end of the experiment; however, the increase was not significant. In group-1 and -2 dogs, IL-6 activities significantly and gradually increased in the systemic and portal circulation during the reperfusion phase, and the magnitude of these increases was dependent on the duration of the ischemic phase. There were no significant changes in IL-1beta activity or endotoxin concentration in any dog group.
Results of the our study indicate that intestinal ischemia and reperfusion leads to significant increases of the circulating TNF-alpha and IL-6 activities, depending on the duration of the ischemia phase, in the absence of detectable endotoxin in the circulation. This finding suggests that intestinal ischemia and reperfusion induces a systemic proinflammatory cytokine response in dogs.
确定小肠缺血再灌注是否会在犬的体循环或门静脉循环中诱导细菌移位和促炎细胞因子反应。
17只健康成年比格犬。
肠系膜上动脉(SMA)分别阻断0分钟(3组犬)、30分钟(1组犬)或60分钟(2组犬),随后再灌注180分钟;在不同时间点测量血清乳酸和内毒素浓度以及体循环和门静脉循环中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和IL-6的活性以及黏膜内pH值。
在2组犬中,发现门静脉循环中TNFα活性显著增加,在再灌注60分钟时达到峰值;体循环中TNF-α活性从再灌注60分钟到实验结束逐渐增加,但增加不显著。在1组和2组犬中,再灌注阶段体循环和门静脉循环中IL-6活性显著且逐渐增加,这些增加的幅度取决于缺血阶段的持续时间。任何犬组中IL-1β活性或内毒素浓度均无显著变化。
我们的研究结果表明,小肠缺血再灌注会导致循环中TNF-α和IL-6活性显著增加,这取决于缺血阶段的持续时间,且循环中未检测到内毒素。这一发现表明小肠缺血再灌注在犬中诱导了全身性促炎细胞因子反应。