Nilsson U A, Aberg J, Aneman A, Lundgren O
Department of Physiology, University of Göteborg, Sweden.
Eur Surg Res. 1993 Jan-Feb;25(1):20-9. doi: 10.1159/000129253.
Experimental ischemia of 15, 30, or 60 min length, followed by 30 min of reperfusion, was produced in situ in the cat small intestine by means of an adjustable arterial clamp. Arterial perfusion pressure was lowered to such an extent that intestinal blood flow decreased from about 25 to 3.5 ml x min-1 x 100 g-1. The rate of free radical formation was followed intermittently with ESR and a modified spin trapping technique in the control period prior to ischemia and at various times during reperfusion. Upon reperfusion radical formation increased above the preischemic control value in all three series of experiments. Cumulative radical production during the 30 min reperfusion period rose from about 3 mumol x 100 g-1 after 15 min ischemia to approximately 4.5 mumol x 100 g-1 after 30 min and 8-10 mumol x 100 g-1 after 60 or 120 min ischemia. At the same time mucosal damage became more pronounced, suggesting a causal connection between tissue damage and radical formation. More specifically, radical production was strongly correlated to histological damage occurring during reperfusion as seen when comparing radical production in animals not experiencing reperfusion damage to those who did. Radical formation in these two groups were 0.35 and 9.0 mumol x 100 g-1, respectively (p < 0.0005).
通过可调节动脉夹在猫小肠原位制造持续15、30或60分钟的实验性缺血，随后再灌注30分钟。动脉灌注压降低到使肠血流量从约25毫升·分钟⁻¹·100克⁻¹降至3.5毫升·分钟⁻¹·100克⁻¹的程度。在缺血前的对照期以及再灌注期间的不同时间，用电子自旋共振（ESR）和改良的自旋捕捉技术间歇性地跟踪自由基形成速率。在所有三个系列的实验中，再灌注时自由基形成增加到缺血前对照值以上。在30分钟再灌注期内，累积自由基产生量从缺血15分钟后的约3微摩尔·100克⁻¹增加到缺血30分钟后的约4.5微摩尔·100克⁻¹，以及缺血60或120分钟后的8 - 10微摩尔·100克⁻¹。与此同时，黏膜损伤变得更加明显，表明组织损伤与自由基形成之间存在因果关系。更具体地说，自由基产生与再灌注期间发生的组织学损伤密切相关，这一点在比较未经历再灌注损伤的动物和经历了再灌注损伤的动物的自由基产生情况时可以看出。这两组中的自由基形成分别为0.35和9.0微摩尔·100克⁻¹（p < 0.0005）。
