Sun J X, Farias L A, Markov A K
Qinghai Medical College, Qinghai Province, Peoples' Republic of China.
Gastroenterology. 1990 Jan;98(1):117-26. doi: 10.1016/0016-5085(90)91299-l.
This study of ischemic and postischemic reperfusion intestinal injury in rats evaluates the potential therapeutic value of fructose 1-6 diphosphate on the basis of its ability to enhance anaerobic carbohydrate metabolism during ischemia and to prevent additional tissue injury after reestablishing blood flow by inhibiting the neutrophils to produce oxygen free radicals. In pursuit of this goal, 28 rats were randomized into 4 groups: pretreated with fructose 1-6 diphosphate (n = 7); pretreated with glucose (n = 7); post-reperfusion treated with fructose 1-6 diphosphate (n = 7); and post-reperfusion treated with saline (n = 7). Five additional rats were sham operated. Following 30 min occlusion of the superior mesenteric artery, all rats received their respective treatments for 5 days. Post-reperfusion arterial pressure was significantly lower in the control rats (p less than 0.001) as well as when compared with the fructose 1-6 diphosphate groups (p less than 0.001). Significant increase in white blood cell counts occurred in the controls (p less than 0.001), whereas in the fructose 1-6 diphosphate groups white blood cell counts were no different from preischemic values. All control rats that died in less than 5 days had transmural intestinal necrosis, whereas in 3 of the controls that survived 5 days, partial intestinal necrosis was noted. Only one fructose 1-6 diphosphate-treated rat had partial intestinal necrosis. The overall 5-day survival was 100% for sham-operated rats, 93% for fructose 1-6 diphosphate-treated rats, and 21% for controls (fructose 1-6 diphosphate vs. controls, p less than 0.001; fructose 1-6 diphosphate vs. sham, NS). The results are discussed and explained in terms of the postulated mechanism based on the pharmacological properties of fructose 1-6 diphosphate.
本研究通过评估1,6 - 二磷酸果糖在大鼠缺血及缺血后再灌注性肠损伤中的作用，探讨其潜在治疗价值。1,6 - 二磷酸果糖可增强缺血时的无氧糖代谢，并通过抑制中性粒细胞产生氧自由基，防止再灌注后额外的组织损伤。为实现这一目标，将28只大鼠随机分为4组：1,6 - 二磷酸果糖预处理组（n = 7）；葡萄糖预处理组（n = 7）；1,6 - 二磷酸果糖再灌注后治疗组（n = 7）；生理盐水再灌注后治疗组（n = 7）。另外5只大鼠进行假手术。在肠系膜上动脉阻断30分钟后，所有大鼠接受各自治疗5天。再灌注后，对照组大鼠的动脉压显著降低（p < 0.001），与1,6 - 二磷酸果糖组相比也显著降低（p < 0.001）。对照组白细胞计数显著增加（p < 0.001），而1,6 - 二磷酸果糖组白细胞计数与缺血前值无差异。所有在5天内死亡的对照大鼠均有透壁性肠坏死，而在存活5天的3只对照大鼠中，发现有部分肠坏死。仅1只接受1,6 - 二磷酸果糖治疗的大鼠有部分肠坏死。假手术大鼠的总体5天生存率为100%，1,6 - 二磷酸果糖治疗组大鼠为93%，对照组为21%（1,6 - 二磷酸果糖组与对照组相比，p < 0.001；1,6 - 二磷酸果糖组与假手术组相比，无显著差异）。根据1,6 - 二磷酸果糖的药理特性所假设的机制，对结果进行了讨论和解释。
