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。