Patterson W R, Padgett G A, Bell T G
Thromb Res. 1985 Jan 1;37(1):61-71. doi: 10.1016/0049-3848(85)90033-7.
Platelets from dogs affected with Basset Hound Hereditary Thrombopathy (BHT), have a thrombasthenia-like aggregation defect but release storage pool ATP in quantities not significantly different from normal controls or BHT heterozygotes when stimulated with 1 X 10(-5)M ADP and 0.22 U/ml thrombin. However, the release occurs so rapidly in the BHT platelets stimulated with ADP that it is complete in approximately one-sixth of the time required for release from normal control and heterozygote platelets. Sequential electron micrographs reveal early release of BHT dense body constituents 30 seconds after stimulation with 1 X 10(-5)M ADP while resting BHT morphology is indistinguishable from normal control animals.
患有巴吉度猎犬遗传性血栓形成症（BHT）的犬只的血小板，具有类似血小板无力症的聚集缺陷，但在用1×10⁻⁵M ADP和0.22 U/ml凝血酶刺激时，其储存池ATP的释放量与正常对照或BHT杂合子无显著差异。然而，在用ADP刺激的BHT血小板中，释放发生得非常迅速，大约只需从正常对照和杂合子血小板释放所需时间的六分之一即可完成。连续电子显微镜图像显示，在用1×10⁻⁵M ADP刺激30秒后，BHT致密体成分早期释放，而静止的BHT形态与正常对照动物无法区分。
