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Increasing hepatic arterial flow to hypovascular hepatic tumours using degradable starch microspheres

机译:使用可降解淀粉微球体增加流向肝下血管肿瘤的肝动脉流量

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The effect of degradable starch microspheres (DSM) on the intrahepatic distribution of a low molecular weight marker, 99Tcm-labelled methylene diphosphonate (MDP), was studied in rats with hypovascular HSN liver tumours. MDP was injected regionally, via the hepatic artery, alone or co-administered with DSM, with or without subsequent occlusion of either the hepatic artery or the portal vein. Tumour vascularity was measured with 57Co-labelled microspheres. Co-injection with DSM immediately significantly increased hepatic retention of marker in both tumour (T) (median 22.40 (range 16.82-39.58)% injected dose) and normal liver (N) (9.08 (4.85-12.59) %ID) the greater effect seen in T (P < 0.01). After DSM degradation, very little MDP remained in N (0.61 (0.28-1.40) %ID) but there was significant retention in T (10.01 (6.73-20.28) %ID, P < 0.01). Clamping the hepatic artery had minimal effect on the retention of MDP when administered alone. Regional injection of 16.5 microM 57Co microspheres resulted in a N:T ratio of 2.25:1. Concomitant injection of the 40 microM DSM was 57Co microspheres reversed this ratio to 1:2. The results indicate that DSM selectively enhances the retention of MDP to a hypovascular hepatic tumour, not by causing intra-tumour stasis, but by directing a greater arterial flow to hypovascular areas in the liver.
机译:在患有血管性HSN肝肿瘤的大鼠中研究了可降解淀粉微球(DSM)对低分子量标记物99Tcm标记的二膦酸二甲酯(MDP)肝内分布的影响。单独或与DSM共同通过肝动脉局部注射MDP,有或没有随后阻塞肝动脉或门静脉。用57 Co标记的微球体测量肿瘤血管。与DSM共同注射可立即显着增加肿瘤(T)(中位22.40(范围16.82-39.58)%注射剂量)和正常肝脏(N)(9.08(4.85-12.59)%ID)中肝标志物的肝滞留在T中观察到更大的效果(P <0.01)。 DSM降解后,几乎没有MDP保留在N中(0.61(0.28-1.40)%ID),但在T中有显着保留(10.01(6.73-20.28)%ID,P <0.01)。单独施用时,夹入肝动脉对MDP的保留影响最小。 16.5 microM 57Co微球的区域注射导致N:T比为2.25:1。伴随注射的40 microM DSM为57Co微球,使该比例逆转为1:2。结果表明,DSM不是通过引起肿瘤内淤滞,而是通过将更大的动脉血流引导至肝脏的血管不足区域,选择性地增强MDP对血管不足的肝肿瘤的保留。

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