Nielsen Vance G, Geary Brian T
Department of Anesthesiology, University of Alabama at Birmingham, 619 South 19th Street, Birmingham, AL 35249, USA.
Transplantation. 2002 Oct 27;74(8):1181-3. doi: 10.1097/00007890-200210270-00021.
Hepatic transplantation may result in coagulopathy caused by the release of mast-cell-derived heparin, and xanthine oxidase (XO) inhibition stabilizes mast cells. Thus, XO inactivation could decrease coagulopathy after hepatoenteric ischemia-reperfusion. Rabbits were fed a standard or XO-inactivating diet before hepatoenteric ischemia for 35 min and before 30 min of reperfusion. Hemostasis was assessed by thrombelastography. Heparin activity was quantified by anti-IIa. XO inactivation resulted in clot formation after reperfusion in all animals, whereas only 37.5% of animals with XO activity clotted (P<0.05). Anti-IIa activity was less in animals at baseline and after reperfusion with XO inactivation (45+/-5 and 65+/-5 mU/mL, respectively) compared to animals with XO activity (51+/-4 and 71+/-5 mU/mL, respectively) (P<0.05). Clot strength, which was mediated by coagulation proteins, was significantly greater at baseline and after reperfusion in animals with XO inactivation. XO inactivation enhances hemostasis by decreasing circulating heparin activity and increasing coagulation protein function before ischemia-reperfusion.
肝移植可能会因肥大细胞源性肝素的释放而导致凝血病，而黄嘌呤氧化酶（XO）抑制可使肥大细胞稳定。因此，XO失活可减轻肝肠缺血再灌注后的凝血病。在对家兔进行35分钟肝肠缺血及30分钟再灌注之前，分别给予其标准饮食或XO失活饮食。通过血栓弹力图评估止血情况。通过抗IIa定量肝素活性。XO失活使所有动物在再灌注后形成血凝块，而具有XO活性的动物只有37.5%形成血凝块（P<0.05）。与具有XO活性的动物（分别为51±4和71±5 mU/mL）相比，XO失活的动物在基线时和再灌注后的抗IIa活性较低（分别为45±5和65±5 mU/mL）（P<0.05）。由凝血蛋白介导的血凝块强度在XO失活的动物基线时和再灌注后明显更大。XO失活通过在缺血再灌注前降低循环肝素活性和增加凝血蛋白功能来增强止血。
