Heyes H, Köhle W, Hilgard P
Thromb Res. 1982 Jun 1;26(5):371-8. doi: 10.1016/0049-3848(82)90255-9.
In rats bearing the solid Walker 256 carcinosarcoma microangiopathic haemolytic anaemia (MHA) developed during the course of tumour growth. A phase of hypercoagulability was followed by a significant decrease in plasma fibrinogen, platelet count and antithrombin III. A diminished haematocrit and a rise in plasma haemoglobin and schistocyte count were accompanied by fibrin deposits in the tumour vessels. When the rats were treated with heparin during the growth of the Walker tumour, both DIC and MHA were prevented except of the last period of the experiment. The tumour sizes, however, did not differ in the controls and the heparinized animals. There is a fair amount of evidence to suggest that the MHA was induced by a tumour-dependent DIC which was blocked by heparin over a certain time period. In contrast, the tumour growth was not modified by effective suppression of DIC and MHA.
在携带实体Walker 256癌肉瘤的大鼠中，肿瘤生长过程中出现了微血管病性溶血性贫血（MHA）。先是出现高凝阶段，随后血浆纤维蛋白原、血小板计数和抗凝血酶III显著降低。血细胞比容降低、血浆血红蛋白升高和裂体细胞计数增加的同时，肿瘤血管中有纤维蛋白沉积。当在Walker肿瘤生长期间用肝素治疗大鼠时，除实验最后阶段外，弥散性血管内凝血（DIC）和MHA均得到预防。然而，对照组和肝素化动物的肿瘤大小并无差异。有大量证据表明，MHA是由肿瘤依赖性DIC诱导的，而肝素在一定时间段内可阻断该过程。相比之下，有效抑制DIC和MHA并未改变肿瘤生长。
