Cosgriff T M, Bunner D P, Wannemacher R W, Hodgson L A, Dinterman R E
Toxicol Appl Pharmacol. 1984 Dec;76(3):454-63. doi: 10.1016/0041-008x(84)90349-1.
T-2 toxin produced significant coagulation abnormalities when administered parenterally to Hartley strain guinea pigs. The animals developed depressed activity of all coagulation factors except fibrinogen. Platelet aggregation in whole blood was depressed in response to ADP and collagen. The animals also exhibited an initial rise followed by a fall in hematocrit level, leukocytosis, and a decrease in platelet count. These changes were detectable within hours of toxin administration, reached a maximum at 24 hr, and returned to normal over the next 2 days. Pretreatment of animals with vitamin K1 had no effect on the activity of coagulation factors. The activated partial thromboplastin time of dilutions of plasma from animals given T-2 toxin with plasma from control animals revealed a pattern which pointed to a deficiency of coagulation factors as the principal cause of prolonged clotting times in treated animals. The presence of a weak circulating anticoagulant could not be ruled out. The addition of T-2 to plasma and blood of normal animals in a concentration of 1 microgram/ml had no effect on clotting times or platelet aggregation.
将T-2毒素经肠胃外途径给予Hartley品系豚鼠时,会产生显著的凝血异常。这些动物除纤维蛋白原外,所有凝血因子的活性均降低。全血中的血小板聚集因二磷酸腺苷(ADP)和胶原蛋白而受到抑制。这些动物还表现出红细胞压积水平先升高后降低、白细胞增多以及血小板计数减少。这些变化在毒素给药数小时内即可检测到,在24小时时达到最大值,并在接下来的2天内恢复正常。用维生素K1对动物进行预处理对凝血因子的活性没有影响。将给予T-2毒素的动物血浆稀释液与对照动物血浆混合后的活化部分凝血活酶时间显示出一种模式,表明凝血因子缺乏是受试动物凝血时间延长的主要原因。不能排除存在微弱循环抗凝剂的可能性。以1微克/毫升的浓度将T-2添加到正常动物的血浆和血液中,对凝血时间或血小板聚集没有影响。