Effect of ischemic-reperfusion injury induced by transient embolization for tumor tissue

在本研究中，兔VX2癌经导管血管造影局部灌注可降解淀粉微球（DSM），证实了DSM阻塞了肿瘤血管。经DSM治疗后，肿瘤内血流迅速下降，恢复到原有水平。我们证明，将DSM输注到喂养肿瘤组织的动脉中可以获得抗肿瘤作用。在单次输注和每天输注30mg/kg DSM 3 d的组中，肿瘤生长比与对照组有显著差异，肿瘤生长受到明显抑制。与对照组相比，每日给药10mg/kg组肿瘤生长受到抑制，连续3 d。本研究测定了注射DSM后肿瘤组织中超氧化物歧化酶（SOD）活性的时间变化。肿瘤组织血流再灌注后，SOD活性值明显降低。在肿瘤周围的肌肉中，观察到SOD活性的同步变化。病理上未见肿瘤血管被血栓阻塞。认为瞬态栓塞剂DSM的抗肿瘤作用是继发于缺血-再灌注损伤现象。

In this study, rabbits with VX2 carcinoma received regional infusion of degradable starch microsphere(DSM) by transcatheter angiography, and it was confirmed that DSM occluded tumor vessels. Blood flow in the tumors decreased rapidly immediately after the DSM treatment and returned to the original level. We demonstrated that the antitumor effect was obtained by the infusion of DSM to the arteries by which the tumor tissues were fed. In the groups given the DSM for 30mg/kg by both single infusion and daily for 3 days, the tumor growth ratio was significantly different from the control group, tumor growth was significantly inhibited. The tumor growth ratio in the group given the DSM for 10mg/kg by daily for 3 days was inhibited to compare with the control group. In this study, the time course changes of the activity of superoxide dismutase(SOD) in the tumoral tissue were measured after injection of the DSM. The value of the activity of SOD was significantly decreased after re-perfusion of tumor tissue blood flow. In the muscles around the tumor, the same time course changes of the activity of SOD were observed.Pathologically, occlusion of the tumor vessels by thrombus was not observed. It was thought that the antitumor effect of the transient embolic agent DSM was secondary to the phenomenon of ischemic-reperfusion injury.