Zoghbi S S, Thakur M L, Sostman H D, Neumann R D, Carbo P, Lord P, Greenspan R H, Gottschalk A
Invest Radiol. 1985 Mar-Apr;20(2):198-202. doi: 10.1097/00004424-198503000-00019.
We investigated the influence of heparin (H) (bolus i.v.; 100-200 I.U./kg.) on the in vivo distribution and accumulation of autologous indium-111-platelets (In-111-P) on experimental pulmonary emboli (PE) in a canine model. Using a thrombin clot formation technique, we induced pulmonary emboli in ten dogs; three dogs were treated with heparin (H), and seven were not (NH). Of five control animals without PE, two were heparinized (H-control) and three were not (NH-control). Animals were sacrificed after 4 to 5 hours of serial blood sampling and sequential scintigraphy. We observed that heparin increased the recovery of In-111-P in the peripheral blood circulation of both control and PE dogs, and reduced the liver uptake of In-111-P in the PE dogs. No PE could be detected while the dogs were fully heparinized, but as the heparin effect dissipated over time, the deposition of In-111-P permitted the scintigraphic detection of PE.
我们研究了肝素（H）（静脉推注；100 - 200国际单位/千克）对犬实验性肺栓塞（PE）模型中自体铟 - 111标记血小板（In - 111 - P）在体内分布和聚集的影响。采用凝血酶凝块形成技术，我们在10只犬中诱导肺栓塞；3只犬接受肝素治疗（H组），7只未接受治疗（NH组）。在5只无PE的对照动物中，2只接受肝素化处理（H - 对照组），3只未接受处理（NH - 对照组）。在连续4至5小时的血液采样和连续闪烁扫描后处死动物。我们观察到，肝素增加了对照犬和PE犬外周血液循环中In - 111 - P的回收率，并降低了PE犬肝脏对In - 111 - P的摄取。在犬完全肝素化时未检测到PE，但随着肝素作用随时间消散，In - 111 - P的沉积使得能够通过闪烁扫描检测到PE。
